2022/05/10 更新

写真a

ミヤハラ ノブアキ
宮原 信明
MIYAHARA Nobuaki
所属
保健学域 教授
職名
教授
外部リンク

学位

  • 医学博士 ( 岡山大学 )

研究キーワード

  • 呼吸器・アレルギー

研究分野

  • ライフサイエンス / 膠原病、アレルギー内科学

  • ライフサイエンス / 呼吸器内科学

  • ライフサイエンス / 呼吸器内科学

 

論文

  • A case of Fulminant Respiratory Failure Caused by Anti-asparaginyl tRNA Synthetase (Anti-KS) Antibody Syndrome-related Interstitial Lung Disease.

    Naohiro Oda, Akihiko Taniguchi, Toshiyuki Aokage, Satoru Senoo, Kenta Nagashima, Reo Mitani, Ichiro Takata, Nobuaki Miyahara

    Internal medicine (Tokyo, Japan)   2022年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Anti-asparaginyl tRNA synthetase (KS) antibodies, detected in <5% patients with anti-aminoacyl-tRNA synthetase antibody syndrome, are strongly associated with interstitial pneumonia but not myositis and skin symptoms. A recent report suggested that most patients with interstitial pneumonia and anti-KS antibody (KS-ILD) may present with chronic disease. We herein report a rare case of severe acute respiratory failure in a KS-ILD patient requiring extracorporeal membrane oxygenation (ECMO). ECMO is useful for facilitating not only lung rest until recovery but also the definitive diagnosis and treatment of ILD. KS-ILD can develop acutely with fulminant respiratory failure, as observed in this case.

    DOI: 10.2169/internalmedicine.9239-21

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  • Identification of targetable kinases in idiopathic pulmonary fibrosis. 国際誌

    Hisao Higo, Kadoaki Ohashi, Shuta Tomida, Sachi Okawa, Hiromasa Yamamoto, Seiichiro Sugimoto, Satoru Senoo, Go Makimoto, Kiichiro Ninomiya, Takamasa Nakasuka, Kazuya Nishii, Akihiko Taniguchi, Toshio Kubo, Eiki Ichihara, Katsuyuki Hotta, Nobuaki Miyahara, Yoshinobu Maeda, Shinichi Toyooka, Katsuyuki Kiura

    Respiratory research   23 ( 1 )   20 - 20   2022年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Tyrosine kinase activation plays an important role in the progression of pulmonary fibrosis. In this study, we analyzed the expression of 612 kinase-coding and cancer-related genes using next-generation sequencing to identify potential therapeutic targets for idiopathic pulmonary fibrosis (IPF). METHODS: Thirteen samples from five patients with IPF (Cases 1-5) and eight samples from four patients without IPF (control) were included in this study. Six of the thirteen samples were obtained from different lung segments of a single patient who underwent bilateral pneumonectomy. Gene expression analysis of IPF lung tissue samples (n = 13) and control samples (n = 8) was performed using SureSelect RNA Human Kinome Kit. The expression of the selected genes was further confirmed at the protein level by immunohistochemistry (IHC). RESULTS: Gene expression analysis revealed a correlation between the gene expression signatures and the degree of fibrosis, as assessed by Ashcroft score. In addition, the expression analysis indicated a stronger heterogeneity among the IPF lung samples than among the control lung samples. In the integrated analysis of the 21 samples, DCLK1 and STK33 were found to be upregulated in IPF lung samples compared to control lung samples. However, the top most upregulated genes were distinct in individual cases. DCLK1, PDK4, and ERBB4 were upregulated in IPF case 1, whereas STK33, PIM2, and SYK were upregulated in IPF case 2. IHC revealed that these proteins were expressed in the epithelial layer of the fibrotic lesions. CONCLUSIONS: We performed a comprehensive kinase expression analysis to explore the potential therapeutic targets for IPF. We found that DCLK1 and STK33 may serve as potential candidate targets for molecular targeted therapy of IPF. In addition, PDK4, ERBB4, PIM2, and SYK might also serve as personalized therapeutic targets of IPF. Additional large-scale studies are warranted to develop personalized therapies for patients with IPF.

    DOI: 10.1186/s12931-022-01940-y

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  • Protective effects of neuropeptide Y against elastase-induced pulmonary emphysema. 国際誌

    Akihiko Taniguchi, Naohiro Oda, Daisuke Morichika, Satoru Senoo, Junko Itano, Utako Fujii, Lili Guo, Ryota Sunami, Katsuyuki Kiura, Yoshinobu Maeda, Nobuaki Miyahara

    American journal of physiology. Lung cellular and molecular physiology   2022年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Neuropeptide Y (NPY) is a neuropeptide widely expressed in not only the central nervous system but also immune cells and the respiratory epithelium. Patients with chronic obstructive pulmonary disease (COPD) reportedly exhibit decreased NPY expression in the airway epithelium, but the involvement of NPY in the pathophysiology of COPD has not been defined. We investigated the role of NPY in elastase-induced emphysema. NPY-deficient (NPY-/-) mice and wild-type (NPY+/+) mice received intratracheal instillation of porcine pancreas elastase (PPE). The numbers of inflammatory cells and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates were determined along with quantitative morphometry of lung sections. Intratracheal instillation of PPE induced emphysematous changes and increased NPY levels in the lungs. Compared with NPY+/+ mice, NPY-/- mice had significantly enhanced PPE-induced emphysematous changes and alveolar enlargement. Neutrophilia seen in BAL flu12id of NPY+/+ mice on day 4 after PPE instillation was also enhanced in NPY-/- mice, and the enhancement was associated with increased levels of neutrophil-related and macrophage-related chemokines and IL-17A as well as increased numbers of type 3 innate lymphoid cells in the airways. Treatment with NPY significantly reduced PPE-induced emphysematous changes. Conversely, treatment with a NPY receptor antagonist exacerbated PPE-induced emphysematous changes. These observations indicate that NPY has protective effects against elastase-induced emphysema, and suggest that targeting NPY in emphysema has potential as a therapeutic strategy for delaying disease progression.

    DOI: 10.1152/ajplung.00353.2020

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  • Nonepisodic angioedema with eosinophilia during sublingual immunotherapy with house dust mite extract. 査読 国際誌

    Naohiro Oda, Takahisa Koyama, Yuki Nakagawa, Nobuaki Miyahara

    Allergology international : official journal of the Japanese Society of Allergology   2021年12月

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    担当区分:最終著者   記述言語:英語  

    DOI: 10.1016/j.alit.2021.11.004

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  • The effects of inhaling hydrogen gas on macrophage polarization, fibrosis, and lung function in mice with bleomycin-induced lung injury. 国際誌

    Toshiyuki Aokage, Mizuki Seya, Takahiro Hirayama, Tsuyoshi Nojima, Masumi Iketani, Michiko Ishikawa, Yasuhiro Terasaki, Akihiko Taniguchi, Nobuaki Miyahara, Atsunori Nakao, Ikuroh Ohsawa, Hiromichi Naito

    BMC pulmonary medicine   21 ( 1 )   339 - 339   2021年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Acute respiratory distress syndrome, which is caused by acute lung injury, is a destructive respiratory disorder caused by a systemic inflammatory response. Persistent inflammation results in irreversible alveolar fibrosis. Because hydrogen gas possesses anti-inflammatory properties, we hypothesized that daily repeated inhalation of hydrogen gas could suppress persistent lung inflammation by inducing functional changes in macrophages, and consequently inhibit lung fibrosis during late-phase lung injury. METHODS: To test this hypothesis, lung injury was induced in mice by intratracheal administration of bleomycin (1.0 mg/kg). Mice were exposed to control gas (air) or hydrogen (3.2% in air) for 6 h every day for 7 or 21 days. Respiratory physiology, tissue pathology, markers of inflammation, and macrophage phenotypes were examined. RESULTS: Mice with bleomycin-induced lung injury that received daily hydrogen therapy for 21 days (BH group) exhibited higher static compliance (0.056 mL/cmH2O, 95% CI 0.047-0.064) than mice with bleomycin-induced lung injury exposed only to air (BA group; 0.042 mL/cmH2O, 95% CI 0.031-0.053, p = 0.02) and lower static elastance (BH 18.8 cmH2O/mL, [95% CI 15.4-22.2] vs. BA 26.7 cmH2O/mL [95% CI 19.6-33.8], p = 0.02). When the mRNA levels of pro-inflammatory cytokines were examined 7 days after bleomycin administration, interleukin (IL)-6, IL-4 and IL-13 were significantly lower in the BH group than in the BA group. There were significantly fewer M2-biased macrophages in the alveolar interstitium of the BH group than in the BA group (3.1% [95% CI 1.6-4.5%] vs. 1.1% [95% CI 0.3-1.8%], p = 0.008). CONCLUSIONS: The results suggest that hydrogen inhalation inhibits the deterioration of respiratory physiological function and alveolar fibrosis in this model of lung injury.

    DOI: 10.1186/s12890-021-01712-2

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  • Reactive Oxygen Species and Antioxidative Defense in Chronic Obstructive Pulmonary Disease. 国際誌

    Akihiko Taniguchi, Mitsuru Tsuge, Nobuaki Miyahara, Hirokazu Tsukahara

    Antioxidants (Basel, Switzerland)   10 ( 10 )   2021年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The respiratory system is continuously exposed to endogenous and exogenous oxidants. Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the airways, leading to the destruction of lung parenchyma (emphysema) and declining pulmonary function. It is increasingly obvious that reactive oxygen species (ROS) and reactive nitrogen species (RNS) contribute to the progression and amplification of the inflammatory responses related to this disease. First, we described the association between cigarette smoking, the most representative exogenous oxidant, and COPD and then presented the multiple pathophysiological aspects of ROS and antioxidative defense systems in the development and progression of COPD. Second, the relationship between nitric oxide system (endothelial) dysfunction and oxidative stress has been discussed. Third, we have provided data on the use of these biomarkers in the pathogenetic mechanisms involved in COPD and its progression and presented an overview of oxidative stress biomarkers having clinical applications in respiratory medicine, including those in exhaled breath, as per recent observations. Finally, we explained the findings of recent clinical and experimental studies evaluating the efficacy of antioxidative interventions for COPD. Future breakthroughs in antioxidative therapy may provide a promising therapeutic strategy for the prevention and treatment of COPD.

    DOI: 10.3390/antiox10101537

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  • Essential role of IL-23 in the development of acute exacerbation of pulmonary fibrosis. 国際誌

    Satoru Senoo, Akihiko Taniguchi, Junko Itano, Naohiro Oda, Daisuke Morichika, Utako Fujii, Lili Guo, Ryota Sunami, Arihiko Kanehiro, Fumiaki Tokioka, Akihiko Yoshimura, Katsuyuki Kiura, Yoshinobu Maeda, Nobuaki Miyahara

    American journal of physiology. Lung cellular and molecular physiology   2021年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Acute exacerbation of idiopathic pulmonary fibrosis has a poor prognosis associated with neutrophilic inflammation. Interleukin-23 is a proinflammatory cytokine involved in neutrophilic inflammation. However, little is known about its role in acute exacerbation of pulmonary fibrosis. This study was performed to determine the role of interleukin-23 in acute exacerbation of pulmonary fibrosis. For assessment of acute exacerbation of pulmonary fibrosis, mice were intratracheally administered bleomycin followed by lipopolysaccharide. Inflammatory cells, cytokine levels, and morphological morphometry of the lungs were analyzed. Cytokine levels were measured in the bronchoalveolar lavage fluid of idiopathic pulmonary fibrosis patients with or without acute exacerbation. Interleukin-23, -17A, and -22 levels were increased in the airway of mice with acute exacerbation of pulmonary fibrosis. Interleukin-23p19-deficient mice with acute exacerbation of pulmonary fibrosis had markedly reduced airway inflammation and fibrosis associated with decreased levels of interleukin-17A and -22 compared with wild-type mice. Treatment with an anti-interleukin-23 antibody attenuated airway inflammation and fibrosis and reduced interleukin-17A and -22 levels in mice with acute exacerbation of pulmonary fibrosis. T helper 17 cells were the predominant source of interleukin-17A in mice with acute exacerbation of pulmonary fibrosis. Interleukin-23 levels in bronchoalveolar lavage fluid tended to be higher in idiopathic pulmonary fibrosis patients with than without acute exacerbation. The data presented here suggest that interleukin-23 is essential for the development of acute exacerbation of pulmonary fibrosis, and that blockade of interleukin-23 may be a new therapeutic strategy for acute exacerbation of pulmonary fibrosis.

    DOI: 10.1152/ajplung.00582.2020

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  • Marginal Zone Lymphoma and Lung Adenocarcinoma with an EGFR Exon 19 E746-S752del Mutation in a Patient with IgG4-related Disease.

    Sachi Okawa, Kammei Rai, Nobuharu Fujii, Yuka Gion, Kiichiro Ninomiya, Yuka Kato, Akihiko Taniguchi, Toshio Kubo, Eiki Ichihara, Kadoaki Ohashi, Nobuaki Miyahara, Katsuyuki Hotta, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Internal medicine (Tokyo, Japan)   60 ( 17 )   2831 - 2837   2021年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    A 68-year-old man presented with a solid mass at the left renal pelvis and ureter with multiple systemic lymphadenopathies and a mass with a cavity in the right lower lobe of the lung. While a transbronchial lung biopsy revealed no malignancy, a biopsy of the renal pelvis showed marginal zone lymphoma with polyclonal IgG4-positive cells. The serum IgG4 level and presence of a bilateral orbital mass suggested Mikulicz disease. The lesions shrank following the administration of steroids. A rebiopsy confirmed lung adenocarcinoma, and its background showed IgG4-positive cells a year later. IgG4-related diseases require careful follow-up because they can be complicated by malignancy.

    DOI: 10.2169/internalmedicine.6470-20

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  • Pulmonary Aspergilloma and Allergic Bronchopulmonary Aspergillosis Following the 2018 Heavy Rain Event in Western Japan: A Case Report.

    Eri Ando, Takamasa Nakasuka, Toshio Kubo, Akihiko Taniguchi, Kiichiro Ninomiya, Yuka Kato, Eiki Ichihara, Kadoaki Ohashi, Kammei Rai, Katsuyuki Hotta, Masaomi Yamane, Nobuaki Miyahara, Masahiro Tabata, Yoshinobu Maeda, Katsuyuki Kiura

    Internal medicine (Tokyo, Japan)   2021年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    A 16-year-old boy with asthma participated in recovery volunteer work following the 2018 heavy rains in Japan. One month later, he experienced chest pain and dyspnea. Chest computed tomography revealed a cavity with a fungal ball, and Aspergillus fumigatus was detected in his bronchoalveolar lavage fluid. He was treated with voriconazole, but new consolidations appeared rapidly. He also experienced allergic bronchopulmonary aspergillosis. After prednisolone prescription, the consolidations improved; however, his asthma worsened. He underwent partial lung resection to avoid allergens, and his symptoms improved. We must recognize cases of infection after a disaster, especially in patients with chronic respiratory diseases.

    DOI: 10.2169/internalmedicine.7124-21

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  • Exacerbation of pulmonary cryptococcosis associated with enhancement of Th2 response in the postpartum period. 国際誌

    Shota Miyoshi, Naohiro Oda, Yuka Gion, Takahiro Taki, Reo Mitani, Ichiro Takata, Akihiko Taniguchi, Yasuharu Sato, Nobuaki Miyahara

    Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy   27 ( 8 )   1248 - 1250   2021年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Cryptococcosis is an invasive mycosis that has become increasingly prevalent in immunocompromised patients. Pregnant women are also one of the risk populations for cryptococcosis. Reversal of Th2 to Th1 response following resolution of immunosuppression during the postpartum period can lead to overt clinical manifestations of a previously silent infection, resembling an immune reconstitution inflammatory syndrome. Here, we report a case of a 30-year-old woman who had an exacerbation of pulmonary cryptococcosis in the postpartum period mimicking an immune reconstitution inflammatory syndrome. In the present case, chest computed tomography showed multiple small nodules on the day of the delivery; however, pulmonary cryptococcosis, which was subclinical during pregnancy, rapidly worsened to mass-like consolidation at one month after the delivery. Pathohistological examination of the lung specimen showed lung parenchyma infiltration with histiocytes and numerous lymphocytes without granulomatous formations, and a small number of yeast-like organisms consistent with Cryptococcus without capillary involvement. Immunohistochemical staining showed predominance of CD3+ cells and CD4+ cells over CD8+ cells. In addition, GATA3+ cells dominated over T-bet + cells. These data suggested exacerbation of pulmonary cryptococcosis associated with enhancement of Th2 response in the postpartum period.

    DOI: 10.1016/j.jiac.2021.03.025

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  • 経食道的気管支鏡下穿刺吸引生検法(EUS-B-FNA)後に縦隔血腫を来した1例

    南 大輔, 柴田 祐作, 中村 香葉, 村上 悦子, 宮原 信明, 岸野 大蔵, 瀧川 奈義夫, 吉川 真生, 田尾 裕之, 水谷 尚雄, 堀田 真智子, 山岡 正和, 廣岡 空良, 石崎 秀美

    姫路赤十字病院誌   45   15 - 18   2021年7月

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    記述言語:日本語   出版者・発行元:姫路赤十字病院図書学術委員会  

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  • Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice. 国際誌

    Daisuke Morichika, Akihiko Taniguchi, Naohiro Oda, Utako Fujii, Satoru Senoo, Junko Itano, Arihiko Kanehiro, Yoshiaki Kitaguchi, Masanori Yasuo, Masayuki Hanaoka, Takashi Satoh, Shizuo Akira, Katsuyuki Kiura, Yoshinobu Maeda, Nobuaki Miyahara

    Respiratory research   22 ( 1 )   150 - 150   2021年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. METHODS: We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33-/- mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. RESULTS: Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33-/- mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33-/- and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33-/- mice than WT mice. IL-33-/- mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. CONCLUSION: These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD.

    DOI: 10.1186/s12931-021-01705-z

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  • Interstitial Pneumonia Secondary to Hermansky-Pudlak Syndrome Type 4 Treated with Different Antifibrotic Agents.

    Junko Itano, Yasushi Tanimoto, Goro Kimura, Noboru Hamada, Hisaaki Tanaka, Shinsuke Ninomiya, Kenjiro Kosaki, Nobuaki Miyahara, Yoshinobu Maeda, Katsuyuki Kiura

    Internal medicine (Tokyo, Japan)   60 ( 5 )   783 - 788   2021年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Hermansky-Pudlak syndrome (HPS) is an autosomal recessive hereditary disease that may be complicated by progressive and potentially fatal interstitial pneumonia. We herein report a 64-year-old woman with interstitial pneumonia associated with HPS type 4 whom we treated with nintedanib after pirfenidone proved ineffective. To our knowledge, there have been no previous reports of nintedanib being used to treat a patient with HPS type 4. There is a need for clinical trials of antifibrotic agents, including nintedanib, pirfenidone, and new therapeutic agents with different mechanisms of action in these patients.

    DOI: 10.2169/internalmedicine.5493-20

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  • Pulmonary epithelioid haemangioendothelioma mimicking lung cancer. 国際誌

    Naohiro Oda, Yoshinobu Maeda, Kastuyuki Kiura, Nobuaki Miyahara

    BMJ case reports   14 ( 2 )   2021年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1136/bcr-2020-240152

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  • The heterodimer S100A8/A9 is a potent therapeutic target for idiopathic pulmonary fibrosis. 国際誌

    Kota Araki, Rie Kinoshita, Nahoko Tomonobu, Yuma Gohara, Shuta Tomida, Yuta Takahashi, Satoru Senoo, Akihiko Taniguchi, Junko Itano, Ken-Ichi Yamamoto, Hitoshi Murata, Ken Suzawa, Kazuhiko Shien, Hiromasa Yamamoto, Mikio Okazaki, Seiichiro Sugimoto, Kouichi Ichimura, Masahiro Nishibori, Nobuaki Miyahara, Shinichi Toyooka, Masakiyo Sakaguchi

    Journal of molecular medicine (Berlin, Germany)   99 ( 1 )   131 - 145   2021年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    In patients with interstitial pneumonia, pulmonary fibrosis is an irreversible condition that can cause respiratory failure. Novel treatments for pulmonary fibrosis are necessary. Inflammation is thought to activate lung fibroblasts, resulting in pulmonary fibrosis. Of the known inflammatory molecules, we have focused on S100A8/A9 from the onset of inflammation to the subsequent progression of inflammation. Our findings confirmed the high expression of S100A8/A9 in specimens from patients with pulmonary fibrosis. An active role of S100A8/A9 was demonstrated not only in the proliferation of fibroblasts but also in the fibroblasts' differentiation to myofibroblasts (the active form of fibroblasts). S100A8/A9 also forced fibroblasts to upregulate the production of collagen. These effects were induced via the receptor of S100A8/A9, i.e., the receptor for advanced glycation end products (RAGE), on fibroblasts. The anti-S100A8/A9 neutralizing antibody inhibited the effects of S100A8/A9 on fibroblasts and suppressed the progression of fibrosis in bleomycin (BLM)-induced pulmonary fibrosis mouse model. Our findings strongly suggest a crucial role of S100A8/A9 in pulmonary fibrosis and the usefulness of S100A8/A9-targeting therapy for fibrosis interstitial pneumonia. HIGHLIGHTS: S100A8/A9 level is highly upregulated in the IPF patients' lungs as well as the blood. S100A8/A9 promotes not only the growth of fibroblasts but also differentiation to myofibroblasts. The cell surface RAGE acts as a crucial receptor to the extracellular S100A8/A9 in fibroblasts. The anti-S100A8/A9 antibody effectively suppresses the progression of IPF in a mouse model. In idiopathic pulmonary fibrosis (IPF), S100A8/A9, a heterodimer composed of S100A8 and S100A9 proteins, plays a crucial role in the onset of inflammation and the subsequent formation of a feed-forward inflammatory loop that promotes fibrosis. (1) The local, pronounced increase in S100A8/A9 in the injured inflammatory lung region-which is provided mainly by the activated neutrophils and macrophages-exerts strong inflammatory signals accompanied by dozens of inflammatory soluble factors including cytokines, chemokines, and growth factors that further act to produce and secrete S100A8/A9, eventually making a sustainable inflammatory circuit that supplies an indefinite presence of S100A8/A9 in the extracellular space with a mal-increased level. (2) The elevated S100A8/A9 compels fibroblasts to activate through receptor for advanced glycation end products (RAGE), one of the major S100A8/A9 receptors, resulting in the activation of NFκB, leading to fibroblast mal-events (e.g., elevated cell proliferation and transdifferentiation to myofibroblasts) that actively produce not only inflammatory cytokines but also collagen matrices. (3) Finally, the S100A8/A9-derived activation of lung fibroblasts under a chronic inflammation state leads to fibrosis events and constantly worsens fibrosis in the lung. Taken together, these findings suggest that the extracellular S100A8/A9 heterodimer protein is a novel mainstay soluble factor for IPF that exerts many functions as described above (1-3). Against this background, we herein applied the developed S100A8/A9 neutralizing antibody to prevent IPF. The IPF imitating lung fibrosis in an IPF mouse model was effectively blocked by treatment with the antibody, leading to enhanced survival. The developed S100A8/A9 antibody, as an innovative novel biologic, may help shed light on the difficulties encountered with IPF therapy in clinical settings.

    DOI: 10.1007/s00109-020-02001-x

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  • Deterioration of high-resolution computed tomography findings predicts disease progression after initial decline in forced vital capacity in idiopathic pulmonary fibrosis patients treated with pirfenidone. 国際誌

    Hisao Higo, Nobuaki Miyahara, Akihiko Taniguchi, Satoru Senoo, Junko Itano, Hiromi Watanabe, Naohiro Oda, Hiroe Kayatani, Hirohisa Ichikawa, Takuo Shibayama, Kazuhiro Kajimoto, Yasushi Tanimoto, Arihiko Kanehiro, Yoshinobu Maeda, Katsuyuki Kiura

    Respiratory investigation   58 ( 3 )   185 - 189   2020年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Pirfenidone suppresses the decline of forced vital capacity (FVC) in patients with idiopathic pulmonary fibrosis (IPF). However, IPF progresses in some patients despite treatment. We analyzed patients with meaningful FVC declines during pirfenidone treatment and explored the factors predictive of disease progression after FVC decline. METHODS: This study was a retrospective, multicenter, observational study conducted by the Okayama Respiratory Disease Study Group. We defined initial decline in %FVC as 5% or greater per 6-month period during pirfenidone treatment. IPF patients who were treated with pirfenidone and experienced an initial decline from December 2008 to September 2017 were enrolled. RESULTS: We analyzed 21 patients with IPF. After the initial decline, 4 (19.0%) patients showed improvement in disease, 11 (52.4%) showed stable disease, and 6 (28.6%) showed progressive disease. There was no significant correlation between %FVC reduction on initial decline and subsequent %FVC change (p = 0.475). Deterioration of high-resolution computed tomography (HRCT) findings on initial decline was observed significantly more often in the progressive versus improved/stable disease groups (100% vs 20.0%, p = 0.009). CONCLUSIONS: We revealed that deterioration of HRCT findings may predict disease progression after the initial decline in %FVC in IPF patients treated with pirfenidone.

    DOI: 10.1016/j.resinv.2019.12.007

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  • Nintedanib can be used safely and effectively for idiopathic pulmonary fibrosis with predicted forced vital capacity ≤ 50%: A multi-center retrospective analysis. 国際誌

    Satoru Senoo, Nobuaki Miyahara, Akihiko Taniguchi, Naohiro Oda, Junko Itano, Hisao Higo, Naofumi Hara, Hiromi Watanabe, Hirohisa Kano, Toshimitsu Suwaki, Yasuko Fuchimoto, Kazuhiro Kajimoto, Hirohisa Ichikawa, Kenichiro Kudo, Takuo Shibayama, Yasushi Tanimoto, Shoichi Kuyama, Arihiko Kanehiro, Yoshinobu Maeda, Katsuyuki Kiura

    PloS one   15 ( 8 )   e0236935   2020年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Nintedanib is a multi-kinase inhibitor approved for idiopathic pulmonary fibrosis (IPF); however, its efficacy and safety for patients with IPF and restricted pulmonary function remain unclear. Therefore, the objective of this study was to determine the efficacy and safety of nintedanib for patients with IPF and forced vital capacity (FVC) ≤ 50%. METHODS: This was a multi-center retrospective study performed by the Okayama Respiratory Disease Study Group. Patients were allocated into FVC ≤ 50% and FVC > 50% groups based on their predicted FVC. The primary endpoints were FVC changes from baseline after 6 and 12 months. RESULTS: 45 patients were eligible for the study. 18 patients had FVC ≤ 50%, and 27 patients had FVC > 50%. Overall, 31 and 19 patients underwent pulmonary function tests at 6 and 12 months after initiating nintedanib, respectively. FVC changes from baseline at 6 and 12 months after initiating nintedanib were comparable between the two groups. Adverse events were seen in all patients, and the rates of patients who discontinued nintedanib were also comparable (38.9% vs. 37.0%, p = 1.000). Multiple regression analysis showed that age and forced expiratory volume in 1 second (FEV1)/FVC were negatively correlated with changes in FVC at 6 months after initiating nintedanib. CONCLUSIONS: Our data suggest that nintedanib can be a useful agent for IPF patients, including those with a low FVC, and that age and FEV1/FVC are predictive markers for changes in FVC following nintedanib treatment.

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  • [The role of neuropeptide Y for the development of allergic airway responses].

    Nobuaki Miyahara

    Nihon yakurigaku zasshi. Folia pharmacologica Japonica   155 ( 6 )   360 - 363   2020年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    Neuropeptide Y (NPY) is a neurotransmitter that is widely expressed in the brain and peripheral nervous system. Various immune cells express the receptor for NPY, Y1 receptor. NPY modulates these cells via its Y1 receptor, and involvement of NPY in the pathophysiology of bronchial asthma, has been reported. Increased plasma levels of NPY in asthmatic patients have been reported. NPY polymorphisms are associated with an increased risk for asthma in overweight subjects and young adults. We and other researchers have reported that using murine models of allergic airway responses, NPY and Y1 receptor play critical roles for the development of allergic airway inflammation and airway hyperresponsiveness. Therefore, manipulating NPY-Y1 pathway represents a novel therapeutic target to control allergic airway responses, and might be beneficial for treatment of bronchial asthma.

    DOI: 10.1254/fpj.20036

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  • Solitary pulmonary nodules caused by Mycobacterium avium complex. 査読 国際誌

    Marukawa M, Taniguchi A, Kimura G, Kunichika N, Kuyama S, Maeda Y, Kiura K, Miyahara N, OKAYAMA Respiratory, Disease Study Group, ORDSG

    Respiratory investigation   57 ( 6 )   566 - 573   2019年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.resinv.2019.07.001

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  • Successful Re-administration of Osimertinib in Osimertinib-induced Interstitial Lung Disease with an Organizing Pneumonia Pattern: A Case Report and Literature Review. 査読

    Itano J, Higo H, Ohashi K, Makimoto G, Nishii K, Hotta K, Miyahara N, Maeda Y, Kiura K

    Internal medicine (Tokyo, Japan)   59 ( 6 )   823 - 828   2019年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.2169/internalmedicine.3689-19

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  • Managing Lung Cancer with Comorbid Interstitial Pneumonia. 査読

    Ichihara E, Miyahara N, Maeda Y, Kiura K

    Internal medicine (Tokyo, Japan)   59 ( 2 )   163 - 167   2019年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.2169/internalmedicine.3481-19

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  • Cause of pleuroparenchymal fibroelastosis following allogeneic hematopoietic stem cell transplantation. 査読 国際誌

    Higo H, Miyahara N, Taniguchi A, Maeda Y, Kiura K

    Respiratory investigation   57 ( 4 )   321 - 324   2019年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.resinv.2019.04.003

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  • Requirement for neuropeptide Y in the development of type 2 responses and allergen-induced airway hyperresponsiveness and inflammation. 査読 国際誌

    Oda N, Miyahara N, Taniguchi A, Morichika D, Senoo S, Fujii U, Itano J, Gion Y, Kiura K, Kanehiro A, Maeda Y

    American journal of physiology. Lung cellular and molecular physiology   316 ( 3 )   L407 - L417   2019年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1152/ajplung.00386.2018

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  • A retinoid X receptor partial agonist attenuates pulmonary emphysema and airway inflammation. 査読 国際誌

    Daisuke Morichika, Nobuaki Miyahara, Utako Fujii, Akihiko Taniguchi, Naohiro Oda, Satoru Senoo, Mikio Kataoka, Mitsune Tanimoto, Hiroki Kakuta, Katsuyuki Kiura, Yoshinobu Maeda, Arihiko Kanehiro

    Respiratory research   20 ( 1 )   2 - 2   2019年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Retinoid X receptors (RXRs) are members of the nuclear receptor (NR) superfamily that mediate signalling by 9-cis retinoic acid, a vitamin A derivative. RXRs play key roles not only as homodimers but also as heterodimeric partners, e.g., for retinoic acid receptors, vitamin D receptors, and peroxisome proliferator-activated receptors. The NR family may also play important roles in the development of emphysema. However, the role of RXRs in the pathogenesis of emphysema is not well defined. METHODS: We developed a novel RXR partial agonist (NEt-4IB) and investigated its effect and mechanism compared to a full agonist (bexarotene) in a murine model of emphysema. For emphysema induction, BALB/c mice received intraperitoneal cigarette smoke extract (CSE) or intratracheal porcine pancreas elastase (PPE). Treatment with RXR agonists was initiated before or after emphysema induction. RESULTS: Treatment with NEt-4IB significantly suppressed the increase in static lung compliance and emphysematous changes in CSE-induced emphysema and PPE-induced established and progressive emphysema. NEt-4IB significantly suppressed PPE-induced neutrophilic airway inflammation and the levels of keratinocyte chemoattractant (KC), C-X-C motif ligand5 (CXCL5), interferon (IFN)-γ and IL-17. NEt-4IB also improved the matrix metalloproteinase-9 (MMP-9)/tissue inhibitor of metalloproteinase-1 (TIMP-1) imbalance and the reduced anti-oxidant activity in bronchoalveolar lavage (BAL) fluid. NEt-4IB suppressed PPE-induced vascular endothelial growth factor (VEGF) expression in the airway. Treatment with NEt-4IB and bexarotene significantly suppressed the increase in static lung compliance and emphysematous changes. However, adverse effects of RXR agonists, including hypertriglyceridemia and hepatomegaly, were observed in bexarotene-treated mice but not in NEt-4IB-treated mice. CONCLUSION: These data suggest that RXRs play crucial roles in emphysema and airway inflammation, and novel partial RXR agonists could be potential therapeutic strategies for the treatment of PPE- and CSE-induced emphysema.

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  • Long-term spontaneous remission with active surveillance in IgG4-related pleuritis: A case report and literature review. 査読 国際誌

    Makimoto G, Ohashi K, Taniguchi K, Soh J, Taniguchi A, Miyahara N, Toyooka S, Yoshino T, Maeda Y, Kiura K

    Respiratory medicine case reports   28   100938 - 100938   2019年

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  • A case of axillary lymphadenitis caused by Mycobacterium intracellulare in an immunocompetent patient. 査読 国際誌

    Itano J, Ohashi K, Senoo S, Oda N, Nishii K, Taniguchi A, Miyahara N, Maeda Y, Kiura K

    Respiratory medicine case reports   28   100947 - 100947   2019年

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  • Severe asthma concomitant with allergic bronchopulmonary aspergillosis successfully treated with mepolizumab. 査読 国際誌

    Oda N, Miyahara N, Senoo S, Itano J, Taniguchi A, Morichika D, Fujii U, Maeda Y, Kiura K, Kanehiro A

    Allergology international : official journal of the Japanese Society of Allergology   67 ( 4 )   521 - 523   2018年10月

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  • Lavender Essential Oil and Its Main Constituents Inhibit the Expression of TNF-α-induced Cell Adhesion Molecules in Endothelial Cells. 査読

    Aoe M, Ueno-Iio T, Shibakura M, Shinohata R, Usui S, Arao Y, Ikeda S, Miyahara N, Tanimoto M, Kataoka M

    Acta medica Okayama   71 ( 6 )   493 - 503   2017年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.18926/AMO/55586

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  • Protective Effects of Bisoprolol against Acute Exacerbation in Moderate-to-Severe Chronic Obstructive Pulmonary Disease 査読

    Akihiko Taniguchi, Nobuaki Miyahara, Naohiro Oda, Daisuke Morichika, Eiki Ichihara, Isao Oze, Yasushi Tanimoto, Hirohisa Ichikawa, Utako Fujii, Mitsune Tanimoto, Arihiko Kanehiro, Katsuyuki Kiura

    ACTA MEDICA OKAYAMA   71 ( 5 )   453 - 457   2017年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Although recent retrospective studies suggested that the use of beta-blockers appears to help improve the mortality rate and decrease the rate of exacerbation in chronic obstructive pulmonary disease (COPD) patients with heart failure, the effects of beta-blockers on COPD patients without heart failure have not been established. Based on previous reports, we have launched a multicenter, prospective, single-arm phase II study to evaluate the preventive effect of the cardioselective beta-blocker bisoprolol in COPD exacerbation, in Japanese individuals with moderate-to-severe COPD who do not have heart failure but do have hypertension requiring the use of medication. The primary endpoint is the rate of mild-to-severe COPD exacerbation. The results of this study will clarify whether bisoprolol can prevent exacerbation in COPD patients without heart failure.

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  • Clinical characteristics of Japanese candidates for lung transplant for interstitial lung disease and risk factors for early death while on the waiting list. 査読 国際誌

    Hisao Higo, Takeshi Kurosaki, Eiki Ichihara, Toshio Kubo, Kentaroh Miyoshi, Shinji Otani, Seiichiro Sugimoto, Masaomi Yamane, Nobuaki Miyahara, Katsuyuki Kiura, Shinichiro Miyoshi, Takahiro Oto

    Respiratory investigation   55 ( 4 )   264 - 269   2017年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Lung transplants have produced very favorable outcomes for patients with interstitial lung disease (ILD) in Japan. However, because of the severe donor lung shortage, patients must wait approximately 2.5 years before they can undergo transplantation and many candidates die before allocation. We reveal the clinical characteristics of Japanese patients with ILD who are candidates for lung transplants and the risk factors for early death while on the waiting list. METHODS: We retrospectively reviewed the clinical data of patients registered in the Japan Organ Transplant Network from Okayama University Hospital who are candidates for cadaveric lung transplants for ILD between 1999 and 2015. RESULTS: Fifty-three patients with ILD were included (24 patients with idiopathic pulmonary fibrosis and 29 others). They had severe pulmonary dysfunction and low exercise tolerability. The median waiting time for transplantation was 462 days, and 22 patients died before allocation. Patients who died before 462 days without undergoing transplantation had more severe dyspnea, shorter 6-minute walk distance (6MWD), and lower performance status than those who waited ≥462 days. CONCLUSIONS: Japanese candidates for cadaveric lung transplants for ILD have severe pulmonary dysfunction. Severe dyspnea, short 6MWD, and low performance status are risk factors for early death while on the waiting list.

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  • Long-term effects of beta-blocker use on lung function in japanese patients with chronic obstructive pulmonary disease 査読

    Naohiro Oda, Nobuaki Miyahara, Hirohisa Ichikawa, Yasushi Tanimoto, Kazuhiro Kajimoto, Makoto Sakugawa, Haruyuki Kawai, Akihiko Taniguchi, Daisuke Morichika, Mitsune Tanimoto, Arihiko Kanehiro, Katsuyuki Kiura

    International Journal of COPD   12   1119 - 1124   2017年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Dove Medical Press Ltd.  

    Background: Some recent studies have suggested that beta-blocker use in patients with chronic obstructive pulmonary disease (COPD) is associated with a reduction in the frequency of acute exacerbations. However, the long-term effects of beta-blocker use on lung function of COPD patients have hardly been evaluated. Patients and methods: We retrospectively reviewed 31 Japanese COPD patients taking beta-blockers for &gt
    1 year and 72 patients not taking them. The association between beta-blocker use and the annual change in forced expiratory volume in 1 second (FEV1) was assessed. Results: At baseline, patient demographic characteristics were as follows: 97 males (mean age 67.0±8.2 years)
    32 current smokers
    and Global Initiative for Chronic Obstructive Lung disease (GOLD) stages I: n=26, II: n=52, III: n=19, and IV: n=6. Patients taking beta-blockers exhibited a significantly lower forced vital capacity (FVC), FEV1, and %FVC, and a more advanced GOLD stage. The mean duration of beta-blocker administration was 2.8±1.7 years. There were no differences in the annual change in FEV1 between patients who did and did not use beta-blockers (-7.6±93.5 mL/year vs -4.7±118.9 mL/year, P=0.671). After controlling for relevant confounders in multivariate analyses, it was found that beta-blocker use was not significantly associated with the annual decline in FEV1 (β=-0.019
    95% confidence interval: -0.073 to 0.036
    P=0.503). Conclusion: Long-term beta-blocker use in Japanese COPD patients might not affect the FEV1, one of the most important parameters of lung function in COPD patients.

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  • Effect of a retinoid X receptor partial agonist on airway inflammation and hyperresponsiveness in a murine model of asthma 査読

    Utako Fujii, Nobuaki Miyahara, Akihiko Taniguchi, Naohiro Oda, Daisuke Morichika, Etsuko Murakami, Hikari Nakayama, Koichi Waseda, Mikio Kataoka, Hiroki Kakuta, Mitsune Tanimoto, Arihiko Kanehiro

    Respiratory Research   18 ( 1 )   23   2017年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BioMed Central Ltd.  

    Background: Retinoid X receptors (RXRs) are members of the nuclear receptor (NR) superfamily that mediate signaling by 9-cis retinoic acid, a vitamin A (retinol) derivative. RXRs play key roles not only as homodimers but also as heterodimeric partners-e.g., retinoic acid receptors (RARs), vitamin D receptors (VDRs), liver X receptors (LXRs), and peroxisome proliferator-activated receptors (PPARs). The NR family was recently associated with allergic diseases, but the role of RXRs in allergen-induced airway responses is not well defined. The goal of this study is to elucidate the role of RXRs in asthma pathogenesis and the potency of RXR partial agonist in the treatment of allergic airway inflammation and airway hyperresponsiveness using a murine model of asthma. Methods: We investigated the effect of a novel RXR partial agonist (NEt-4IB) on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in a murine model of asthma. Balb/c mice were sensitized (days 0 and 14) and challenged (days 28-30) with ovalbumin (OVA), and airway inflammation and airway responses were monitored 48 h after the last OVA challenge. NEt-4IB was administered orally on days 25 to 32. Results: Oral administration of NEt-4IB significantly suppressed AHR and inflammatory cell accumulation in the airways and attenuated the levels of TNF-α in the lung and IL-5, IL-13 and NO levels in bronchoalveolar lavage (BAL) fluid and the number of periodic acid Schiff (PAS)-positive goblet cells in lung tissue. Treatment with NEt-4IB also significantly suppressed NF-ΚB expression. Conclusion: These data suggest that RXRs may be of crucial importance in the mechanism of allergic asthma and that the novel RXR partial agonist NEt-4IB may be a promising candidate for the treatment of allergic airway inflammation and airway hyperresponsiveness in a model of allergic asthma.

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  • Effect of a retinoid X receptor partial agonist on airway inflammation and hyperresponsiveness in a murine model of asthma 査読

    Utako Fujii, Nobuaki Miyahara, Akihiko Taniguchi, Naohiro Oda, Daisuke Morichika, Etsuko Murakami, Hikari Nakayama, Koichi Waseda, Mikio Kataoka, Hiroki Kakuta, Mitsune Tanimoto, Arihiko Kanehiro

    RESPIRATORY RESEARCH   18   2017年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BIOMED CENTRAL LTD  

    Background: Retinoid X receptors (RXRs) are members of the nuclear receptor (NR) superfamily that mediate signaling by 9-cis retinoic acid, a vitamin A (retinol) derivative. RXRs play key roles not only as homodimers but also as heterodimeric partners-e.g., retinoic acid receptors (RARs), vitamin D receptors (VDRs), liver X receptors (LXRs), and peroxisome proliferator-activated receptors (PPARs). The NR family was recently associated with allergic diseases, but the role of RXRs in allergen-induced airway responses is not well defined. The goal of this study is to elucidate the role of RXRs in asthma pathogenesis and the potency of RXR partial agonist in the treatment of allergic airway inflammation and airway hyperresponsiveness using a murine model of asthma.
    Methods: We investigated the effect of a novel RXR partial agonist (NEt-4IB) on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in a murine model of asthma. Balb/c mice were sensitized (days 0 and 14) and challenged (days 28-30) with ovalbumin (OVA), and airway inflammation and airway responses were monitored 48 h after the last OVA challenge. NEt-4IB was administered orally on days 25 to 32.
    Results: Oral administration of NEt-4IB significantly suppressed AHR and inflammatory cell accumulation in the airways and attenuated the levels of TNF-a in the lung and IL-5, IL-13 and NO levels in bronchoalveolar lavage (BAL) fluid and the number of periodic acid Schiff (PAS)-positive goblet cells in lung tissue. Treatment with NEt-4IB also significantly suppressed NF-.B expression.
    Conclusion: These data suggest that RXRs may be of crucial importance in the mechanism of allergic asthma and that the novel RXR partial agonist NEt-4IB may be a promising candidate for the treatment of allergic airway inflammation and airway hyperresponsiveness in a model of allergic asthma.

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  • Pneumocystis Pneumonia Concomitant with Ectopic ACTH Syndrome Caused by a Large Cell Neuroendocrine Carcinoma of the Thymus 査読

    Naohiro Oda, Nobuaki Miyahara, Masahiro Tabata, Daisuke Minami, Kiichiro Ninomiya, Arihiko Kanehiro, Motoshi Komatsubara, Kenichi Inagaki, Mitsune Tanimoto, Katsuyuki Kiura

    INTERNAL MEDICINE   56 ( 5 )   551 - 555   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPAN SOC INTERNAL MEDICINE  

    We herein report the case of a 44-year-old man who was diagnosed with pneumocystis pneumonia (PCP) concomitant with ectopic adrenocorticotropic hormone (ACTH) syndrome, which had been caused by a large cell neuroendocrine carcinoma of the thymus. Chest computed tomography revealed ground-glass opacities in the lungs. PCP was diagnosed by a polymerase chain reaction with bronchoalveolar lavage. The levels of cortisol were slowly corrected with an adrenal enzyme inhibitor, and the exacerbation of PCP was successfully avoided. Our case indicates that in addition to prophylaxis, the early diagnosis of PCP and the slow correction of hypercortisolemia should be considered in order to prevent an exacerbation due to the reconstitution of the immune function in patients with ectopic ACTH syndrome.

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  • Long-term effects of beta-blocker use on lung function in Japanese patients with chronic obstructive pulmonary disease 査読

    Naohiro Oda, Nobuaki Miyahara, Hirohisa Ichikawa, Yasushi Tanimoto, Kazuhiro Kajimoto, Makoto Sakugawa, Haruyuki Kawai, Akihiko Taniguchi, Daisuke Morichika, Mitsune Tanimoto, Arihiko Kanehiro, Katsuyuki Kiura

    INTERNATIONAL JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE   12   1119 - 1124   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:DOVE MEDICAL PRESS LTD  

    Background: Some recent studies have suggested that beta-blocker use in patients with chronic obstructive pulmonary disease (COPD) is associated with a reduction in the frequency of acute exacerbations. However, the long-term effects of beta-blocker use on lung function of COPD patients have hardly been evaluated.
    Patients and methods: We retrospectively reviewed 31 Japanese COPD patients taking beta-blockers for &gt;1 year and 72 patients not taking them. The association between beta-blocker use and the annual change in forced expiratory volume in 1 second (FEV1) was assessed.
    Results: At baseline, patient demographic characteristics were as follows: 97 males (mean age 67.0 +/- 8.2 years); 32 current smokers; and Global Initiative for Chronic Obstructive Lung disease (GOLD) stages I: n=26, II: n=52, III: n=19, and IV: n=6. Patients taking beta-blockers exhibited a significantly lower forced vital capacity (FVC), FEV1, and %FVC, and a more advanced GOLD stage. The mean duration of beta-blocker administration was 2.8 +/- 1.7 years. There were no differences in the annual change in FEV1 between patients who did and did not use beta-blockers (-7.6 +/- 93.5 mL/year vs -4.7 +/- 118.9 mL/year, P=0.671). After controlling for relevant confounders in multivariate analyses, it was found that beta-blocker use was not significantly associated with the annual decline in FEV1 (beta=-0.019; 95% confidence interval: -0.073 to 0.036; P=0.503).
    Conclusion: Long-term beta-blocker use in Japanese COPD patients might not affect the FEV1, one of the most important parameters of lung function in COPD patients.

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  • IL-23 Is Essential for the Development of Elastase-Induced Pulmonary Inflammation and Emphysema 査読

    Utako Fujii, Nobuaki Miyahara, Akihiko Taniguchi, Koichi Waseda, Daisuke Morichika, Etsuko Kurimoto, Hikari Koga, Mikio Kataoka, Erwin W. Gelfand, Daniel J. Cua, Akihiko Yoshimura, Mitsune Tanimoto, Arihiko Kanehiro

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   55 ( 5 )   697 - 707   2016年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    We recently reported that IL-17A plays a critical role in the development of porcine pancreatic elastase (PPE)-induced emphysema. The proliferation of T-helper type 17 (Th17) cells was induced by IL-23. To determine the contribution of IL-23 to the development of pulmonary emphysema, a mouse model of PPE-induced emphysema was used in which responses of IL-23p19-deficient (IL-23(-/-)) and wild-type (WT) mice were compared. Intratracheal instillation of PPE induced emphysematous changes in the lungs and was associated with increased levels of IL-23 in lung homogenates. Compared with WT mice, IL-23(-/-) mice developed significantly lower static compliance values and markedly reduced emphysematous changes on histological analyses after PPE instillation. These changes were associated with lower levels of IL-17A and fewer Th17 cells in the lung. The neutrophilia seen in bronchoalveolar lavage fluid ofWTmice was attenuated in IL-23(-/-) mice, and the reduction was associated with decreased levels of keratinocyte-derived cytokine and macrophage inflammatory protein-2 in bronchoalveolar lavage fluid. Treatment with anti-IL-23p40 monoclonal antibody significantly attenuated PPE-induced emphysematous changes in the lungs of WT mice. These data identify the important contributions of IL-23 to the development of elastase-induced pulmonary inflammation and emphysema, mediated through an IL-23/IL-17 pathway. Targeting IL-23 in emphysema is a potential therapeutic strategy for delaying disease progression.

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  • 挿管チューブを使用したEBUS-TBNA後の発熱および穿刺針洗浄培養の後方視的検討

    南 大輔, 瀧川 奈義夫, 二宮 崇, 久保 寿夫, 大橋 圭明, 堀田 勝幸, 柴山 卓夫, 宮原 信明, 田端 雅弘, 谷本 光音, 木浦 勝行

    肺癌   56 ( 6 )   511 - 511   2016年11月

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    記述言語:日本語   出版者・発行元:(NPO)日本肺癌学会  

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  • Heerfordt's Syndrome Associated with a High Fever and Elevation of TNF-α. 査読

    Makimoto G, Miyahara N, Yoshikawa M, Taniguchi A, Kanehiro A, Tanimoto M, Kiura K

    Acta medica Okayama   70 ( 4 )   273 - 277   2016年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Increased Serum KL-6 Levels Induced by Pulmonary Mycobacterium Avium Complex Infection in a Patient with RA-associated Lung Disease 査読

    Koichi Waseda, Kazuki Ocho, Kou Hasegawa, Kosuke Kimura, Masaya Iwamuro, Yoshihisa Hanayama, Eisei Kondo, Nobuaki Miyahara, Fumio Otsuka

    ACTA MEDICA OKAYAMA   70 ( 3 )   217 - 221   2016年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    KL-6 is a glycoprotein found predominantly on type II pneumocytes and alveolar macrophages, and often shows increased serum levels in patients with interstitial pneumonia. We report a case of mycobacterium avium complex (MAC) infection whose disease activity was correlated with KL-6 levels in serum. During treatment of rheumatoid arthritis (RA)-associated interstitial lung disease (ILD) with prednisolone, chest image findings improved in association with decreased KL-6 levels. Following tapering of prednisolone, chest image findings deteriorated again as levels of KL-6 increased, suggesting recurrence of RA-ILD. Bronchoscopic examination revealed active MAC infection. Treatment of MAC infection not only improved chest image findings but also decreased KL-6 levels in serum, suggesting that KL-6 was increased by active MAC infection by itself, not by recurrence of RA-ILD. To the best of our knowledge, this is the first documentation of KL-6 elevation in serum in association with active MAC infection.

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  • Immunomodulatory Effects of Ambroxol on Airway Hyperresponsiveness and Inflammation 査読

    Katsuyuki Takeda, Nobuaki Miyahara, Shigeki Matsubara, Christian Taube, Kenichi Kitamura, Astushi Hirano, Mitsune Tanimoto, Erwin W. Gelfand

    IMMUNE NETWORK   16 ( 3 )   165 - 175   2016年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:KOREA ASSOC IMMUNOLOGISTS  

    Ambroxol is used in COPD and asthma to increase mucociliary clearance and regulate surfactant levels, perhaps through anti-oxidant and anti-inflammatory activities. To determine the role and effect of ambroxol in an experimental model of asthma, BALB/c mice were sensitized to ovalbumin (OVA) followed by 3 days of challenge. Airway hyperresponsiveness (AHR), lung cell composition and histology, and cytokine and protein carbonyl levels in bronchoalveolar lavage (BAL) fluid were determined. Ambroxol was administered either before the first OVA challenge or was begun after the last allergen challenge. Cytokine production levels from lung mononuclear cells (Lung MNCs) or alveolar macrophages (AM) were also determined. Administration of ambroxol prior to challenge suppressed AHR, airway eosinophilia, goblet cell metaplasia, and reduced inflammation in subepithelial regions. When given after challenge, AHR was suppressed but without effects on eosinophil numbers. Levels of IL-5 and IL-13 in BAL fluid were decreased when the drug was given prior to challenge; when given after challenge, increased levels of IL-10 and IL-12 were detected. Decreased levels of protein carbonyls were detected in BAL fluid following ambroxol treatment after challenge. In vitro, ambroxol increased levels of IL-10, IFN-gamma, and IL-12 from Lung MNCs and AM, whereas IL-4, IL-5, and IL-13 production was not altered. Taken together, ambroxol was effective in preventing AHR and airway inflammation through upregulation of Th1 cytokines and protection from oxidative stress in the airways.

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  • A case of acquired hemophilia a diagnosed in conjunction with oral bleeding 査読

    Eriko Yanagi, Toshiyuki Kishi, Takao Matsumura, Yoshinori Tani, Nobuaki Miyahara

    Journal of Otolaryngology of Japan   119 ( 8 )   1133 - 1136   2016年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Oto-Rhino-Laryngological Society of Japan Inc.  

    Acquired hemophilia A is a rare disease in which autoantibodies to factor VIII are present. It is often manifested as a sudden onset of a critical bleeding episode, and its incidence is reported to be 1.48 cases per million persons per year. We report herein on a case of acquired hemophilia A associated with a submucosal hematoma of the oral floor, pharynx, and larynx. A 78-year-old male presented with fresh bleeding from his mouth, associated with hematoma of the oral floor, pharynx, and larynx. Laboratory test showed that the activated partial thromboplastin time was prolonged, and the platelet count and prothrombin time were normal. Coagulation tests revealed decreased factor VIII levels, and the presence of factor VIII inhibitor. A diagnosis of acquired hemophilia A was made, and immunotherapy with corticosteroids was initiated. After treatment, the bleeding tendency was controlled. On hospital day 29, the symptoms disappeared. Although acquired hemophilia A is a rare coagulopathic condition, it should be considered as one of the differential diagnoses in a case of sudden onset of severe hemorrhagic tendency of unknown origin.

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  • 肺類上皮血管内皮腫の1例

    田中 晶平, 小田 尚廣, 佐藤 晃子, 宮原 信明, 狩野 裕久, 中西 将元, 秦 雄介, 槇本 剛, 久保 寿夫, 大橋 圭明, 二宮 崇, 堀田 勝幸, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行, 牧 佑歩, 宗 淳一, 豊岡 伸一, 三好 新一郎

    肺癌   55 ( 7 )   1127 - 1127   2015年12月

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    記述言語:日本語   出版者・発行元:(NPO)日本肺癌学会  

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  • Contrasting roles for the receptor for advanced glycation end-products on structural cells in allergic airway inflammation vs. airway hyperresponsiveness 査読

    Akihiko Taniguchi, Nobuaki Miyahara, Koichi Waseda, Etsuko Kurimoto, Utako Fujii, Yasushi Tanimoto, Mikio Kataoka, Yasuhiko Yamamoto, Erwin W. Gelfand, Hiroshi Yamamoto, Mitsune Tanimoto, Arihiko Kanehiro

    AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY   309 ( 8 )   L789 - L800   2015年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    The receptor for advanced glycation end-products (RAGE) is a multiligand receptor that belongs to the immunoglobulin superfamily. RAGE is reported to be involved in various inflammatory disorders; however, studies that address the role of RAGE in allergic airway disease are inconclusive. RAGE-sufficient (RAGE(+/+)) and RAGE-deficient (RAGE(-/-)) mice were sensitized to ovalbumin, and airway responses were monitored after ovalbumin challenge. RAGE(-/-) mice showed reduced eosinophilic inflammation and goblet cell metaplasia, lower T helper type 2 (Th2) cytokine production from spleen and peribronchial lymph node mononuclear cells, and lower numbers of group 2 innate lymphoid cells in the lung compared with RAGE(+/+) mice following sensitization and challenge. Experiments using irradiated, chimeric mice showed that the mice expressing RAGE on radio-resistant structural cells but not hematopoietic cells developed allergic airway inflammation; however, the mice expressing RAGE on hematopoietic cells but not structural cells showed reduced airway inflammation. In contrast, absence of RAGE expression on structural cells enhanced innate airway hyperresponsiveness (AHR). In the absence of RAGE, increased interleukin (IL)-33 levels in the lung were detected, and blockade of IL-33 receptor ST2 suppressed innate AHR in RAGE(-/-) mice. These data identify the importance of RAGE expressed on lung structural cells in the development of allergic airway inflammation, T helper type 2 cell activation, and group 2 innate lymphoid cell accumulation in the airways. RAGE on lung structural cells also regulated innate AHR, likely through the IL-33-ST2 pathway. Thus manipulating RAGE represents a novel therapeutic target in controlling allergic airway responses.

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  • Emphysema Requires the Receptor for Advanced Glycation End-Products Triggering on Structural Cells 査読

    Koichi Waseda, Nobuaki Miyahara, Akihiko Taniguchi, Etsuko Kurimoto, Genyo Ikeda, Hikari Koga, Utako Fujii, Yasuhiko Yamamoto, Erwin W. Gelfand, Hiroshi Yamamoto, Mitsune Tanimoto, Arihiko Kanehiro

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   52 ( 4 )   482 - 491   2015年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Pulmonary emphysema is characterized by persistent inflammation and progressive alveolar destruction. The receptor for advanced glycation end-products (RAGE) is a multiligand cell surface receptor reported to be involved in the process of acute alveolar epithelial cell injury. However, studies that address the role of RAGE in pulmonary emphysema are inconclusive. We investigated the role of RAGE in the development of elastase-induced pulmonary inflammation and emphysema in mice. RAGE-sufficient (RAGE(+/+)) mice and RAGE-deficient (RAGE(-/-)) mice were treated with intratracheal elastase on Day 0. Airway inflammation, static lung compliance, lung histology, and the levels of neutrophil-related chemokine and proinflammatory cytokines in bronchoalveolar lavage fluid were determined on Days 4 and 21. Neutrophilia in bronchoalveolar lavage fluid, seen in elastase-treated RAGE(+/+) mice, was reduced in elastase-treated RAGE(-/-) mice on Day 4, and was associated with decreased levels of keratinocyte chemoattractant, macrophage inflammatory protein-2, and IL-1 beta. Static lung compliance values and emphysematous changes in the lung tissue were decreased in RAGE(-/-) mice compared with RAGE(+/+) mice on Day 21 after elastase treatment. Experiments using irradiated, bone marrow-chimeric mice showed that the mice expressing RAGE on radioresistant structural cells, but not hematopoietic cells, developed elastase-induced neutrophilia and emphysematous change in the lung. In contrast, mice expressing RAGE on hematopoietic cells, but not radioresistant structural cells, showed reduced neutrophilia and emphysematous change in the lung. These data identify the importance of RAGE expressed on lung structural cells in the development of elastase-induced pulmonary inflammation and emphysema. Thus, RAGE represents a novel therapeutic target for preventing pulmonary emphysema.

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  • Effect of a Cysteinyl Leukotriene Receptor Antagonist on Experimental Emphysema and Asthma Combined with Emphysema 査読

    Genyo Ikeda, Nobuaki Miyahara, Hikari Koga, Yasuko Fuchimoto, Koichi Waseda, Etsuko Kurimoto, Akihiko Taniguchi, Yasushi Tanimoto, Mikio Kataoka, Mitsune Tanimoto, Arihiko Kanehiro

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   50 ( 1 )   18 - 29   2014年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    The incidence of overlapping bronchial asthma and chronic obstructive pulmonary disease has increased in recent years. Cysteinyl leukotrienes (CysLTs) play an important role in asthma, and the type 1 CysLT receptor (CysLT(1)R) is expressed by many inflammatory cells. We evaluated the effect of montelukast, a CysLT(1)R antagonist, on mouse models of asthma, porcine pancreatic elastase (PPE)-induced emphysema, and asthma combined with emphysema. Mice were sensitized with ovalbumin (OVA) on Days 0 and 14 and subsequently challenged with OVA on Days 28, 29, and 30. Pulmonary emphysema was induced by intratracheal instillation of PPE on Day 25. Mice were treated subcutaneously with montelukast or vehicle from Day 25 to Day 31. Airway hyperresponsiveness (AHR), static compliance; the number of inflammatory cells, the levels of cytokines, chemokines, LTs, and perforin in the bronchoalveolar lavage fluid, and the quantitative morphometry of lung sections were analyzed on Day 32. Treatment with montelukast significantly attenuated the AHR and eosinophilic airway inflammation in OVA-sensitized and OVA-challenged mice. Administration of montelukast significantly reduced the AHR, static compliance, and neutrophilic airway inflammation, while attenuating emphysematous lung changes, in PPE-treated mice. In PPE-treated mice subjected to allergen sensitization and challenges, montelukast significantly suppressed the AHR, static compliance, and eosinophilic and neutrophilic airway inflammation in addition to the development of experimentally induced emphysema in the lungs. Our data suggest that CysLT(1)R antagonists may be effective in ameliorating the consequences of PPE-induced lung damage and the changes that follow allergen sensitization and challenges.

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  • Invasive Mucinous Adenocarcinoma Mimicking Organizing Pneumonia Associated with Mycobacterium fortuitum Infection 査読

    Daisuke Morichika, Nobuaki Miyahara, Katsuyuki Hotta, Yoshiko Okamoto, Daisuke Minami, Masahiro Irie, Yasushi Tanimoto, Arihiko Kanehiro, Mitsune Tanimoto, Katsuyuki Kiura

    INTERNAL MEDICINE   53 ( 24 )   2795 - 2799   2014年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPAN SOC INTERNAL MEDICINE  

    We herein report the case of a 68-year-old man diagnosed with invasive mucinous adenocarcinoma of the lungs. Chest computed tomography showed subpleural ground-glass opacity and small nodules with cavitation. A culture of the bronchoalveolar lavage fluid resulted in the detection of Mycobacterium fortuitum. The patient's lung consolidation rapidly progressed; however, repeated bronchoscopy showed no atypical cells, thus suggesting a diagnosis of organizing pneumonia associated with M. fortuitum infection. However, the surgical biopsy specimen was diagnostic for adenocarcinoma, with no mycobacterial infection. Invasive mucinous adenocarcinoma should not be excluded in the differential diagnosis of patients with clinical features of organizing pneumonia and nontuberculous mycobacterium infection, even if a transbronchial biopsy confirms the absence of malignancy.

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  • Inhibition of neutrophil elastase attenuates airway hyperresponsiveness and inflammation in a mouse model of secondary allergen challenge: Neutrophil elastase inhibition attenuates allergic airway responses 査読

    Hikari Koga, Nobuaki Miyahara, Yasuko Fuchimoto, Genyo Ikeda, Koichi Waseda, Katsuichiro Ono, Yasushi Tanimoto, Mikio Kataoka, Erwin W. Gelfand, Mitsune Tanimoto, Arihiko Kanehiro

    Respiratory Research   14 ( 1 )   8   2013年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Background: Chronic asthma is often associated with neutrophilic infiltration in the airways. Neutrophils contain elastase, a potent secretagogue in the airways, nonetheless the role for neutrophil elastase as well as neutrophilic inflammation in allergen-induced airway responses is not well defined. In this study, we have investigated the impact of neutrophil elastase inhibition on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in previously sensitized and challenged mice.Methods: BALB/c mice were sensitized and challenged (primary) with ovalbumin (OVA). Six weeks later, a single OVA aerosol (secondary challenge) was delivered and airway inflammation and airway responses were monitored 6 and 48 hrs later. An inhibitor of neutrophil elastase was administered prior to secondary challenge.Results: Mice developed a two-phase airway inflammatory response after secondary allergen challenge, one neutrophilic at 6 hr and the other eosinophilic, at 48 hr. PAR-2 expression in the lung tissues was enhanced following secondary challenge, and that PAR-2 intracellular expression on peribronchial lymph node (PBLN) T cells was also increased following allergen challenge of sensitized mice. Inhibition of neutrophil elastase significantly attenuated AHR, goblet cell metaplasia, and inflammatory cell accumulation in the airways following secondary OVA challenge. Levels of IL-4, IL-5 and IL-13, and eotaxin in BAL fluid 6 hr after secondary allergen challenge were significantly suppressed by the treatment. At 48 hr, treatment with the neutrophil elastase inhibitor significantly reduced the levels of IL-13 and TGF-β1 in the BAL fluid. In parallel, in vitro IL-13 production was significantly inhibited in spleen cells from sensitized mice.Conclusion: These data indicate that neutrophil elastase plays an important role in the development of allergic airway inflammation and hyperresponsiveness, and would suggest that the neutrophil elastase inhibitor reduced AHR to inhaled methacholine indicating the potential for its use as a modulator of the immune/inflammatory response in both the neutrophil- and eosinophil-dominant phases of the response to secondary allergen challenge. © 2013 Koga et al.
    licensee BioMed Central Ltd.

    DOI: 10.1186/1465-9921-14-8

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  • IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice 査読

    Etsuko Kurimoto, Nobuaki Miyahara, Arihiko Kanehiro, Koichi Waseda, Akihiko Taniguchi, Genyo Ikeda, Hikari Koga, Hisakazu Nishimori, Yasushi Tanimoto, Mikio Kataoka, Yoichiro Iwakura, Erwin W. Gelfand, Mitsune Tanimoto

    Respiratory Research   14 ( 1 )   5   2013年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Background: Pulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it's role in the inflammatory response of elastase-induced emphysema remains unclear.Methods: In a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine and pro-inflammatory cytokines in bronchoalveolar lavage (BAL) fluid.Results: Wild-type mice developed emphysematous changes in the lung tissue on day 21 after elastase treatment, whereas emphysematous changes were decreased in IL-17A-deficient mice compared to wild-type mice. Neutrophilia in BAL fluid, seen in elastase-treated wild-type mice, was reduced in elastase-treated IL-17A-deficient mice on day 4, associated with decreased levels of KC, MIP-2 and IL-1 beta. Elastase-treated wild-type mice showed increased IL-17A levels as well as increased numbers of IL-17A+ CD4 T cells in the lung in the initial period following elastase treatment.Conclusions: These data identify the important contribution of IL-17A in the development of elastase-induced pulmonary inflammation and emphysema. Targeting IL-17A in emphysema may be a potential therapeutic strategy for delaying disease progression. © 2013 Kurimoto et al.
    licensee BioMed Central Ltd.

    DOI: 10.1186/1465-9921-14-5

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  • Inhibition of neutrophil elastase attenuates airway hyperresponsiveness and inflammation in a mouse model of secondary allergen challenge: neutrophil elastase inhibition attenuates allergic airway responses 査読

    Hikari Koga, Nobuaki Miyahara, Yasuko Fuchimoto, Genyo Ikeda, Koichi Waseda, Katsuichiro Ono, Yasushi Tanimoto, Mikio Kataoka, Erwin W. Gelfand, Mitsune Tanimoto, Arihiko Kanehiro

    RESPIRATORY RESEARCH   14   2013年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BIOMED CENTRAL LTD  

    Background: Chronic asthma is often associated with neutrophilic infiltration in the airways. Neutrophils contain elastase, a potent secretagogue in the airways, nonetheless the role for neutrophil elastase as well as neutrophilic inflammation in allergen-induced airway responses is not well defined. In this study, we have investigated the impact of neutrophil elastase inhibition on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in previously sensitized and challenged mice.
    Methods: BALB/c mice were sensitized and challenged (primary) with ovalbumin (OVA). Six weeks later, a single OVA aerosol (secondary challenge) was delivered and airway inflammation and airway responses were monitored 6 and 48 hrs later. An inhibitor of neutrophil elastase was administered prior to secondary challenge.
    Results: Mice developed a two-phase airway inflammatory response after secondary allergen challenge, one neutrophilic at 6 hr and the other eosinophilic, at 48 hr. PAR-2 expression in the lung tissues was enhanced following secondary challenge, and that PAR-2 intracellular expression on peribronchial lymph node (PBLN) T cells was also increased following allergen challenge of sensitized mice. Inhibition of neutrophil elastase significantly attenuated AHR, goblet cell metaplasia, and inflammatory cell accumulation in the airways following secondary OVA challenge. Levels of IL-4, IL-5 and IL-13, and eotaxin in BAL fluid 6 hr after secondary allergen challenge were significantly suppressed by the treatment. At 48 hr, treatment with the neutrophil elastase inhibitor significantly reduced the levels of IL-13 and TGF-beta 1 in the BAL fluid. In parallel, in vitro IL-13 production was significantly inhibited in spleen cells from sensitized mice.
    Conclusion: These data indicate that neutrophil elastase plays an important role in the development of allergic airway inflammation and hyperresponsiveness, and would suggest that the neutrophil elastase inhibitor reduced AHR to inhaled methacholine indicating the potential for its use as a modulator of the immune/inflammatory response in both the neutrophil-and eosinophil-dominant phases of the response to secondary allergen challenge.

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  • A Definite Case of L-carbocisteine-induced Pneumonia with CATCH22 Syndrome 査読

    Kenichiro Kudo, Eiki Ichihara, Akiko Hisamoto, Katsuyuki Hotta, Nobuaki Miyahara, Yasushi Tanimoto, Sadaharu Akagi, Katsuya Kato, Mitsune Tanimoto, Katsuyuki Kiura

    INTERNAL MEDICINE   52 ( 1 )   97 - 100   2013年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPAN SOC INTERNAL MEDICINE  

    A 32-year-old male with CATCH22 syndrome presented with a high fever and productive cough after taking drugs for acute bronchitis, including L-carbocisteine. Chest radiography revealed ground-glass opacities in the bilateral lung fields. He had a history of similar pneumonia. Under the assumption of drug-induced pneumonia, or bacterial or viral pneumonia, all drugs including L-carbocisteine were discontinued, and antibiotics were started. A drug-induced lymphocyte stimulation test was positive only for L-carbocisteine. The only drug in common between this and the previous episode of pneumonia was L-carbocisteine. We thus concluded that this was a definite case of L-carbocisteine-induced pneumonia in a patient with CATCH22 syndrome.

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  • [Bronchial asthma and allergic diseases]. 査読

    Miyahara N, Kiura K

    Nihon rinsho. Japanese journal of clinical medicine   70 Suppl 8   545 - 549   2012年11月

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  • Successful Extracorporeal Life Support for Life-threatening Hypercapnia with Bronchiolitis Obliterans after Allogeneic Hematopoietic Stem Cell Transplantation 査読

    Koichi Waseda, Yasushi Tanimoto, Shingo Ichiba, Nobuaki Miyahara, Toshi Murakami, Nobuaki Ochi, Michihisa Terado, Osamu Nagano, Yoshinobu Maeda, Arihiko Kanehiro, Yoshihito Ujike, Mitsune Tanimoto

    ACTA MEDICA OKAYAMA   65 ( 6 )   403 - 406   2011年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Bronchiolitis obliterans (BO) is a disease with a poor prognosis, and a key factor that limits long-term survival after allogeneic hematopoietic stem cell transplantation (HSCT). We here report a case of a 31-year woman with acute lymphatic leukemia, which was treated by chemotherapy and HSCT, and consequently developed BO 2 years after HSCT. A non-tuberculous mycobacterial infection occurred and showed gradual exacerbation. She started taking anti-mycobacterial drugs, but lost appetite, felt tired and finally lost consciousness one month after beginning medication. Arterial blood gas revealed marked hypercapnia. Using extracorporeal life support (ECLS), the carbon dioxide concentration was reduced and her consciousness recovered. To our knowledge, this is the first case in which ECLS was successfully used for hypercapnia in a patient with BO.

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  • Requirement for Chemokine Receptor 5 in the Development of Allergen-Induced Airway Hyperresponsiveness and Inflammation 査読

    Yasuko Fuchimoto, Arihiko Kanehiro, Nobuaki Miyahara, Hikari Koga, Genyo Ikeda, Koichi Waseda, Yasushi Tanimoto, Satoshi Ueha, Mikio Kataoka, Erwin W. Gelfand, Mitsune Tanimoto

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   45 ( 6 )   1248 - 1255   2011年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Chemokine receptor (CCR) 5 is expressed on dendritic cells, macrophages, CD8 cells, memory CD4 T cells, and stromal cells, and is frequently used as a marker of T helper type 1 cells. Interventions that abrogate CCR5 or interfere with its ligand binding have been shown to alter T helper type 2-induced inflammatory responses. The role of CCR5 on allergic airway responses is not defined. CCR5-deficient (CCR5(-/-)) and wild-type (CCR5(+/+)) mice were sensitized and challenged with ovalbumin (OVA) and allergic airway responses were monitored 48 hours after the last OVA challenge. Cytokine levels in lung cell culture supernatants were also assessed. CCR5(-/-) mice showed significantly lower airway hyperresponsiveness (AHR) and lower numbers of total cells, eosinophils, and lymphocytes in bronchoalveolar lavage (BAL) fluid compared with CCR5(+/+) mice after sensitization and challenge. The levels of IL-4 and IL-13 in BAL fluid of CCR5(-/-) mice were lower than in CCR5(+/+) mice. Decreased numbers of lung T cells were also detected in CCR5(-/-) mice after sensitization and challenge. Transfer of OVA-sensitized T cells from CCR5(+/+), but not transfer of CCR5(-/-) cells, into CCR5(-/-) mice restored AHR and numbers of eosinophils in BAL fluid after OVA challenge. Accordingly, the numbers of airway-infiltrating donor T cells were significantly higher in the recipients of CCR5(+/+) T cells. Taken together, these data suggest that CCR5 plays a pivotal role in allergen-induced AHR and airway inflammation, and that CCR5 expression on T cells is essential to the accumulation of these cells in the airways.

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  • Blocking the Leukotriene B4 Receptor 1 Inhibits Late-Phase Airway Responses in Established Disease 査読

    Koichi Waseda, Nobuaki Miyahara, Arihiko Kanehiro, Genyo Ikeda, Hikari Koga, Yasuko Fuchimoto, Etsuko Kurimoto, Yasushi Tanimoto, Mikio Kataoka, Mitsune Tanimoto, Erwin W. Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   45 ( 4 )   851 - 857   2011年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Most of the studies investigating the effectiveness of blocking the leukotriene B4 (LTB4) receptor 1 (BLT1) have been performed in models of primary or acute allergen challenge. The role of the LTB4-BLT1 pathway in secondary challenge models, where airway hyperresponsiveness (AHR) and airway inflammation have been established, has not been defined. We investigated the effects of blocking BLT1 on early-and late-phase development of AHR and airway inflammation in previously sensitized and challenged mice. Female BALB/c mice were sensitized (Days 1 and 14) and challenged (primary, Days 28-30) with ovalbumin. On Day 72, mice were challenged (secondary) with a single OVA aerosol, and the early and late phases of AHR and inflammation were determined. Specific blockade of BLT1 was attained by oral administration of a BLT1 antagonist on Days 70 through 72. Administration of the antagonist inhibited the secondary ovalbumin challenge-induced alterations in airway responses during the late phase but not during the early phase, as demonstrated by decreases in AHR and in bronchoalveolar lavage neutrophilia and eosinophilia 6 and 48 hours after secondary challenge. The latter was associated with decreased levels of KC protein, macrophage inflammatory protein 2, and IL-17 in the airways. These data identify the importance of the LTB4-BLT1 pathway in the development of late-phase, allergen-induced airway responsiveness after secondary airway challenge in mice with established airway disease.

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  • Churg-Strauss Syndrome with Necrosis of Toe Tips 査読

    Koichi Waseda, Yasushi Tanimoto, Kenjiro Hasegawa, Nobuaki Miyahara, Daisuke Nojima, Genyo Ikeda, Arihiko Kanehiro, Chiharu Okada, Yoshihiro Kimata, Mitsune Tanimoto

    ACTA MEDICA OKAYAMA   65 ( 3 )   215 - 218   2011年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Churg-Strauss syndrome (CSS) is a granulomatous necrotizing vasculitis of unknown etiology associated with bronchial asthma. Despite affecting small to medium-sized vessels, necrosis of the digits due to vasculitis is extremely rare. We report a case of CSS with necrosis of the toe tips. A 37-year-old woman with asthma, who had been diagnosed with CSS 2 years ago, was admitted to our hospital with an exacerbation of CSS. The patient had a high grade fever and complained of abdominal pain and numbness of the lower extremities. Blood examination revealed marked eosinophilia. The fever pattern, abdominal pain and blood eosinophilia showed improvement by combination treatment with prednisolone and cyclophosphamide. However, the color of her right toe tips changed, and necrosis finally resulted despite antithrombotic therapy. Arteriography showed narrowing of the dorsalis pedis artery and of the more peripheral arteries of her right leg. Stump plasty with negative pressure dressing therapy for the toe tips, but not amputation, was done to preserve the leg function. While numbness of the extremities remained, no recurrence of necrosis was seen. Clinicians need to be aware that rare complications of CSS, including necrosis of the digits, can occur.

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  • Measurement of early-phase, late-phase, and nonspecific nasal responses in allergic rhinitis mouse by whole body plethysmography. 査読

    Miyahara S, Miyahara N, Matsubara S

    Nihon yakurigaku zasshi. Folia pharmacologica Japonica   137 ( 3 )   141 - 145   2011年3月

  • The relationships between the peak inspiratory flow and the characteristics factors in the asthmatics with inhaled corticosteroid - A multicenter study in Chugoku Shikoku area 査読

    Yasushi Obase, Arihiko Kanehiro, Yasushi Tanimoto, Nobuaki Miyahara, Mikio Oka, Ryosuke Eda, Tetsuya Kubota, Akihito Yokoyama, Kiryo Wakabayashi, Hiroyasu Takeyama, Chiharu Okada, Goro Kimura, Ryo Soda, Kiyoshi Takahashi, Mitsune Tanimoto

    Japanese Journal of Allergology   60 ( 12 )   1621 - 1629   2011年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    Background: Inhaled corticosteroid (ICS) will be effective if used properly. Inadequate intake may result in insufficiency, such as for elderly asthmatics, in particular, for use of dry powder inhalers. Methods: 312 asthmatics treated with ICS for at least 6 months in the 6 facilities belonging to the Chugoku Shikoku Adult Asthma Research Forum were subject to investigation of the peak inspiratory flow (PIF) measured using In-check® and related factors. Results: Nine (2.8%) patients were considered to have insufficient intake. By multivariate analysis, PIF (L/min) prediction formula was as follows: 79.0 + 0.19*peak expiratory flow (PEF: L/min) + 22.9*FVC (L) - 0.68*onset age (years) + 34.7*gender (male, 1
    female, 0) + 16.1*V50/V25, [r∧2 = 0.677, p&lt
    0.0001]. Using cluster analysis with Euclidean distance and Ward's method, the PIF without an adaptor was included in the same category as height and PEF, and the PIF with an adaptor was included in the same category as %FVC and %FEV 10. Conclusion: The cases with insufficient PIF are few but present. Adequate device selection and inhalation guidance may be important. The meaning of PIF differs depending on whether or not an adaptor is present. Further investigation of intake is considered necessary. ©2011 Japanese Society of Allergology.

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  • Plasticity of Invariant NKT Cell Regulation of Allergic Airway Disease Is Dependent on IFN-gamma Production 査読

    Hiroyuki Matsuda, Katsuyuki Takeda, Toshiyuki Koya, Masakazu Okamoto, Yoshiki Shiraishi, Nobuaki Miyahara, Azzeddine Dakhama, Jennifer L. Matsuda, Laurent Gapin, Erwin W. Gelfand

    JOURNAL OF IMMUNOLOGY   185 ( 1 )   253 - 262   2010年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Invariant NKT cells (iNKT cells) play a pivotal role in the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation. However, it is unclear what role they play in the initiation (sensitization) phase as opposed to the effector (challenge) phase. The role of iNKT cells during sensitization was examined by determining the response of mice to intratracheal transfer of OVA-pulsed or OVA-alpha-galactosylceramide (OVA/alpha GalCer)-pulsed bone marrow-derived dendritic cells (BMDCs) prior to allergen challenge. Wild-type (WT) recipients of OVA-BMDCs developed AHR, increased airway eosinophilia, and increased levels of Th2 cytokines in bronchoalveolar lavage fluid, whereas recipients of OVA/alpha GalCer BMDCs failed to do so. In contrast, transfer of these same OVA/alpha GalCer BMDCs into IFN-gamma-deficient (IFN-gamma(-/-)) mice enhanced the development of these lung allergic responses, which was reversed by exogenous IFN-gamma treatment following OVA-BMDC transfer. Further, J alpha 18deficient recipients, which lack iNKT cells, developed the full spectrum of lung allergic responses following reconstitution with highly purified WT liver or spleen iNKT cells and transfer of OVA-BMDCs, whereas reconstituted recipients of OVA/alpha GalCer BMDCs failed to do so. Transfer of iNKT cells from IFN-gamma(-/-) mice restored the development of these responses in J alpha 18-deficient recipients following OVA-BMDC transfer; the responses were enhanced following OVA/alpha GalCer BMDC transfer. iNKT cells from these IFN-gamma(-/-) mice produced higher levels of IL-13 in vitro compared with WT iNKT cells. These data identify IFN-gamma as playing a critical role in dictating the consequences of iNKT cell activation in the initiation phase of the development of AHR and airway inflammation. The Journal of Immunology, 2010, 185: 253-262.

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  • Effects of combination therapy with montelukast and carbocysteine in allergen-induced airway hyperresponsiveness and airway inflammation 査読

    Takeda K, Shiraishi Y, Matsubara S, Miyahara N, Matsuda H, Okamoto M, Joetham A, Gelfand E.W

    British Journal of Pharmacology   160 ( 6 )   1399 - 1407   2010年7月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/j.1476-5381.2010.00797.x

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  • Experimental Pulmonary Granuloma Mimicking Sarcoidosis Induced by Propionibacterium acnes in Mice 査読

    Kouji Iio, Tomoe Ueno Iio, Yuhei Okui, Hirohisa Ichikawa, Yasushi Tanimoto, Nobuaki Miyahara, Arihiko Kanehiro, Mitsune Tanimoto, Yasunari Nakata, Mikio Kataoka

    ACTA MEDICA OKAYAMA   64 ( 2 )   75 - 83   2010年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Propionibacterium acnes has been implicated as an etiologic agent of sarcoidosis since the isolation of this bacterium from sarcoid lesions. We experimentally produced a murine pulmonary granuloma model using P. acnes with several features that simulate sarcoidosis. Mice were sensitized with heat-killed P. acnes and complete Freund's adjuvant and were subsequently challenged with heat-killed P. acnes at 2-week intervals. P. acnes-challenged mice developed epitheloid cell granulomas in the lungs. These mice showed a pulmonary immune response characterized by an increased number of T-lymphocytes, especially CD4+ cells, and the ratio of CD4+/CD8+ in bronchoalveolar lavage (BAL) fluid also increased. Furthermore, significant elevations in both angiotensin-converting enzyme (ACE) serum levels and antibody titers against P. acnes were observed. Mice sensitized with P. acnes without complete Freund's adjuvant were capable of forming pulmonary granulomas, which appeared to be caused by indigenous P. acnes. The genome of P. acnes was found in the lungs, BAL cells, hilar lymph nodes, liver, and spleen in non-sensitized mice, which were thought to be germ-free. These results suggest that the immune response against indigenous P. acnes may play an important role in the pathogenesis of granuloma formation in a murine model.

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  • Diffuse alveolar hemorrhage with chronic thyroiditis in an advanced-age adult 査読

    Masanori Fujii, Nobuaki Miyahara, Yasushi Tanimoto, Nagio Takigawa, Masahiro Tabata, Arihiko Kanehiro, Katsuyuki Kiura, Mitsune Tanimoto

    Respiratory Medicine CME   3 ( 2 )   90 - 92   2010年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Idiopathic pulmonary hemosiderosis (IPH) is one of the rare causes of diffuse alveolar hemorrhage (DAH), and usually occurs in children. The mechanism underlying this disease development has not been defined. During the acute phase, death due to massive alveolar hemorrhage and subsequent severe respiratory failure with multiple organ failure often occurs. We report a case of IPH which occurred in an advanced-aged adult during following thyroidectomy for chronic thyroiditis. Following surgery this 83-year-old male developed acute onset dyspnea and pulmonary hemorrhage. In a search for underlying causes, no disorders were found and the only finding was the presence of anti-thyroid antibody. Systemic corticosteroid therapy was effective and he fully recovered. To our knowledge, this is the second documentation of IPH in association with chronic thyroiditis. © 2009 Elsevier Ltd.

    DOI: 10.1016/j.rmedc.2009.04.006

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  • Differential Effects of Dendritic Cell Transfer on Airway Hyperresponsiveness and Inflammation 査読

    Toshiyuki Koya, Hiroyuki Matsuda, Shigeki Matsubara, Nobuaki Miyahara, Azzeddine Dakhama, Katsuyuki Takeda, Erwin W. Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   41 ( 3 )   271 - 280   2009年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Dendritic cells (DCs) are considered to be the most efficient antigen-presenting cells. Intratracheal administration of allergen-pulsed bone marrow-derived dendritic cells (BMDCs) before allergen challenge induces airway hyperresponsiveness (AHR) and inflammation. Ovalbumin (OVA)-pulsed BMDCs from wild-type (WT) mice were transferred into naive WT, CD4(-/-), CD8(-/-), or IL-13(-/-) mice. Two days (short protocol) or 10 days (long protocol) after BMDC transfer, mice were challenged with 1% OVA for 3 days and assayed 2 days later. Transfer of OVA-primed BMDCs into BALB/c or C57BL/6 mice elicited AHR in both protocols. Airway eosinophilia, Th2 cytokines, or goblet cell metaplasia were increased in the long but not short protocol. Lung T cells from both protocols produced Th2 cytokines in response to OVA in vitro. Carboxyfluorescein diacetate succinimidylester-labeled BMDCs were observed in bronchoalveolar lavage (BAL) fluid and lung parenchyma at early time points, and were detected in draining lymph nodes 48 hours after transfer. CD8(-/-) mice developed AHR comparable to WT mice in the short protocol, but decreased levels of AHR, airway eosinophilia, Th2 cytokines in BAL fluid, and goblet cell metaplasia compared with WT mice in the long protocol. CD4(-/-) or IL-13(-/-) mice did not develop AHR or airway inflammation in either protocol. These data suggest that allergen-pulsed BMDCs initiate development of AHR that is dependent initially on CD4(+) T cells, and at later time periods on CD8+ T cells and IL-13. Thus, the timing of allergen challenge after transfer of allergen-pulsed BMDC affects the development of AHR and airway inflammation.

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  • 気管支喘息 動物モデル 肥満細胞およびロイコトリエンB4の気道過敏性における役割の検討 査読

    宮原 信明, 大西 広志, 金廣 有彦, 早稲田 公一, 池田 元洋, 古賀 光, 渕本 康子, 栗本 悦子, 能島 大輔, 谷本 安, 片岡 幹男, Gelfand Erwin, 谷本 光音

    アレルギー   58 ( 8-9 )   1247 - 1247   2009年9月

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    記述言語:日本語   出版者・発行元:(一社)日本アレルギー学会  

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  • アレルギー疾患と脂質メディエーター 最近の知見 ロイコトリエンB4 査読

    宮原 信明, 大西 広志, 武田 勝行, 宮原 聡子, 早稲田 公一, 池田 元洋, 古賀 光, 渊本 康子, 栗本 悦子, 金廣 有彦, Gelfand Erwin, 谷本 光音

    アレルギー   58 ( 8-9 )   1154 - 1154   2009年9月

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    記述言語:日本語   出版者・発行元:(一社)日本アレルギー学会  

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  • Vaccine-Induced CD8(+) T Cell-Dependent Suppression of Airway Hyperresponsiveness and Inflammation 査読

    Katsuyuki Takeda, Steven W. Dow, Nobuaki Miyahara, Taku Kodama, Toshiyuki Koya, Christian Taube, Anthony Joetham, Jung-Won Park, Azzeddine Dakhama, Ross M. Kedl, Erwin W. Gelfand

    JOURNAL OF IMMUNOLOGY   183 ( 1 )   181 - 190   2009年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Suppressing the abnormalities associated with asthma has been difficult to accomplish using immunotherapy or vaccination once the disease is established. The effector cells necessary for effective immunization/vaccination and immunotherapy of asthma are also not well understood. Therefore, we vaccinated allergen (OVA)-sensitized mice to determine whether therapeutic immunization could suppress airway hyperresponsiveness (AHR) and inflammation and to identify key immune effector cells and cytokines. Mice were immunized with a vaccine comprised of Ag and cationic liposome-DNA complexes (CLDC), a vaccine which has previously been shown to elicit strong CD4(+) and CD8(+) T cell responses and activation of Th1 immunity. We showed that immunization with the OVA-CLDC vaccine significantly suppressed AHR, eosinophilia, goblet cell metaplasia, and Th2 cytokine production. In contrast, immunization with CLDC alone suppressed eosinophilia and Th2 cytokine production, but failed to suppress AHR and goblet cell changes. Using adoptive transfer experiments, we found that suppression of AHR was mediated by Ag-specific CD8(+) T cells and was dependent on IFN-gamma production by the transferred T cells. Thus, we conclude that generation of strong, allergen-specific CD8(+) T cell responses by immunization may be capable of suppressing AHR and allergic airway inflammation, even in previously sensitized and challenged mice. The Journal of Immunology, 2009, 183: 181-190.

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  • Leukotriene B4 Release from Mast Cells in IgE-Mediated Airway Hyperresponsiveness and Inflammation 査読

    Nobuaki Miyahara, Hiroshi Ohnishi, Satoko Miyahara, Katsuyuki Takeda, Shigeki Matsubara, Hiroyuki Matsuda, Masakazu Okamoto, Joan E. Loader, Anthony Joetham, Mitsune Tanimoto, Azzeddine Dakhama, Erwin W. Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   40 ( 6 )   672 - 682   2009年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Previous studies have shown that leukotriene B4 (LTB4), a proinflammatory lipid mediator, is linked to the development of airway hyperresponsiveness through the accumulation of IL-13-producing CD8+ T cells, which express a high affinity receptor for LTB4, BLT1 (Miyahara et al., Am J Respir Crit Care Med 2005;172:161-167; J Immunol 2005;174:4979-4984). By using leukotriene A4 hydrolase-deficient (LTA4H-/-) mice, which fail to synthesize LTB4, we determined the role of this lipid mediator in allergen-induced airway responses. Two approaches were used. In the first, LTA4H-/- mice and wild-type (LTA4H+/+) mice were systemically sensitized and challenged via the airways to ovalbumin. In the second, mice were passively sensitized with anti-ovalbumin IgE and exposed to ovalbumin via the airways. Mast cells were generated from bone marrow of LTA4H+/+ mice or LTA4H-/- mice. After active sensitization and challenge, LTA4H-/- mice showed significantly lower airway hyperresponsiveness compared with LTA4H+/+ mice, and eosinophil numbers and IL-13 levels in the bronchoalveoloar lavage, of LTA4H-/- mice were also significantly lower. LTA4H-/- mice also showed decreased airway reactivity after passive sensitization and challenge. After LTA4H+/+ mast cell transfer, LTA4H-/- mice showed increased airway reactivity after passive sensitization and challenge, but not after systemic sensitization and challenge. These data confirm the important role for LTB4 in the development of altered airway responses and suggest that LTB4 secretion from mast cells is critical to eliciting increased airway reactivity after passive sensitization with allergen-specific IgE.

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  • Allergic Airway Hyperresponsiveness-Enhancing gamma delta T Cells Develop in Normal Untreated Mice and Fail to Produce IL-4/13, Unlike Th2 and NKT Cells 査読

    Niyun Jin, Christina L. Roark, Nobuaki Miyahara, Christian Taube, M. Kemal Aydintug, J. M. Wands, Yafei Huang, Youn-Soo Hahn, Erwin W. Gelfand, Rebecca L. O&apos;Brien, Willi K. Born

    JOURNAL OF IMMUNOLOGY   182 ( 4 )   2002 - 2010   2009年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Allergic airway hyperresponsiveness (AHR) in OVA-sensitized and challenged mice, mediated by allergen-specific Th2 cells and Th2-like invariant NKT (iNKT) cells, develops under the influence of enhancing and inhibitory gamma delta T cells. The AHR-enhancing cells belong to the V gamma 1(+) gamma delta T cell subset, cells that are capable of increasing IL-5 and IL-13 levels in the airways in a manner like Th2 cells. They also synergize with iNKT cells in mediating AHR. However, unlike Th2 cells, the AHR enhancers arise in untreated mice, and we show here that they exhibit their functional bias already as thymocytes, at an HSA(high) maturational stage. In further contrast to Th2 cells and also unlike iNKT cells, they could not be stimulated to produce IL-4 and IL-13, consistent with their synergistic dependence on iNKT cells in mediating AHR. Mice deficient in IFN-gamma, TNFRp75, or IL-4 did not produce these AHR-enhancing gamma delta T cells, but in the absence of IFN-gamma, spontaneous development of these cells was restored by adoptive transfer of IFN-gamma-competent dendritic cells from untreated donors. The i.p. injection of OVA/aluminum hydroxide restored development of the AHR enhancers in all of the mutant strains, indicating that the enhancers still can be induced when they fail to develop spontaneously, and that they themselves need not express TNFRp75, IFN-gamma, or IL-4 to exert their function. We conclude that both the development and the cytokine potential of the AHR-enhancing gamma delta T cells differs critically from that of Th2 cells and NKT cells, despite similar influences of these cell populations on AHR. The Journal of Immunology, 2009, 182: 2002-2010.

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  • Mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2-dependent pathways are essential for CD8(+) T cell-mediated airway hyperresponsiveness and inflammation 査読

    Hiroshi Ohnishi, Katsuyuki Takeda, Joanne Domenico, Joseph J. Lucas, Nobuaki Miyahara, Christina H. Swasey, Azzeddine Dakhama, Erwin W. Gelfand

    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY   123 ( 1 )   249 - 257   2009年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY-ELSEVIER  

    Background: Ligation of the leukotriene B-4 (LTB4) receptor I on effector memory CD8(+) T cells by LTB4 is important for the recruitment of CD8(+) T cells into the airways, which appears central to the induction of airway hyperresponsiveness (AHR) and allergic inflammation. Phosphorylation of extracellular signal-regulated kinase (ERK) is important in activation and cytokine production from many cell types.
    Objective: The roles of ERKs in effector CD8(+) T-cell function and on CD8(+) T cell-mediated AHR were determined.
    Methods: Effector CD8(+) T cells were generated from OVA(257.264) (SIINFEKL) peptide-primed mononuclear cells from OT-1 mice. The effects of U0126, an ERK inhibitor, on effector CD8(+) T-cell function and on CD8(+) T cell-mediated AHR and allergic inflammation were examined.
    Results: Pretreatment of effector CD8(+) T cells with U0126 suppressed anti-CD3/anti-CD28-induced ERK1/2 phosphorylation and cytokine production, but did not affect LTB4-induced Ca2+ mobilization or chemotaxis. Adoptive transfer of U0126-treated CD8(+) T cells into sensitized mice before secondary allergen challenge resulted in significant decreases in AHR, eosinophilic inflammation, goblet cell metaplasia, and IL-5 and IL-13 levels in bronchoalveolar lavage fluid of recipient mice. The number of transferred CD8(+) T cells accumulating in bronchoalveolar lavage fluid or lungs was unaffected by treatment.
    Conclusion: ERK1/2-dependent pathways are essential for the effector functions of CD8(+) T cells, including T(H)2 cytokine production, allergic inflammation, and development of AHR. Inhibition of ERK1/2 signaling has potential therapeutic benefit in preventing CD8(+) T cell-mediated AHR. (J Allergy Clin Immunol 2009;123:249-57.)

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  • Leukotriene B(4) receptor 1 expression on dendritic cells is required for the development of Th2 responses and allergen-induced airway hyperresponsiveness 査読

    Nobuaki Miyahara, Hiroshi Ohnishi, Hiroyuki Matsuda, Satoko Miyahara, Katsuyuki Takeda, Toshiyuki Koya, Shigeki Matsubara, Masakazu Okamoto, Azzeddine Dakhama, Bodduluri Haribabu, Erwin W. Gelfand

    JOURNAL OF IMMUNOLOGY   181 ( 2 )   1170 - 1178   2008年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Dendritic cells (DC) are important APCs that control allergen-induced airway responses by interacting directly with T cells. Leukotriene B(4) (LTB(4)), interacting with its high-affinity receptor, LTB4 receptor 1 (BLT1), is known to attract and activate leukocytes during inflammation. We have previously shown that BLT1 expression on Ag-primed T cells is required for the development of airway hyperresponsiveness (AHR; Miyahara et al. 2005. Am. J. Respir. Crit. Care Med. 172: 161-167). However, the role for the LTB(4)-BLT1 pathway in DC function in allergen-induced airway responses has not been defined. Bone marrow-derived DCs (BMDC) were generated. Naive BALB/c mice received OVA-pulsed BLT1-deficient (BLTI(-/-)) BMDCs or wild-type BMDCs intratracheally and were then challenged with OVA for 3 days. Airway responses were monitored 48 h after the last allergen challenge. BLTI(-/-) BMDCs showed normal maturation judged from surface expression of CD markers. Compared with recipients of wild-type BMDCs, mice that received BLT1(-/-) BMDCs developed significantly lower AHR to inhaled methacholine, lower goblet cell metaplasia, and eosinophilic infiltration in the airways and decreased levels of Th2 type cytokines in the bronchoalveolar lavage fluid. Migration of BLTI(-/-) BMDCs into peribronchial lymph nodes was significantly impaired compared with BLTI(+/+) BMDCs after intratracheal instillation. These data suggest that BLTI expression on DCs is required for migration of DCs to regional lymph nodes as well as in the development of AHR and airway inflammation.

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  • Evidence that CD8(+) dendritic cells enable the development of gamma delta T cells that modulate airway hyperresponsiveness 査読

    Laura Cook, Nobuaki Miyahara, Niyun Jin, J. M. Wands, Christian Taube, Christina L. Roark, Terry A. Potter, Erwin W. Gelfand, Rebecca L. O&apos;Brien, Willi K. Born

    JOURNAL OF IMMUNOLOGY   181 ( 1 )   309 - 319   2008年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Airway hyperresponsiveness (AHR), a hallmark of asthma and several other diseases, can be modulated by gamma delta T cells. In mice sensitized and challenged with OVA, AHR depends on allergen-specific alpha beta T cells; but V gamma 1(+) gamma delta T cells spontaneously enhance AHR, whereas V gamma 4(+) gamma delta T cells, after being induced by airway challenge, suppress AHR. The activity of these gamma delta T cell modulators is allergen nonspecific, and how they develop is unclear. We now show that CD8 is essential for the development of both the AHR suppressor and enhancer gamma delta T cells, although neither type needs to express CD8 itself. Both cell types encounter CD8-expressing non-T cells in the spleen, and their functional development in an otherwise CD8-negative environment can be restored with transferred spleen cell preparations containing CD8(+) dendritic cells (DCs), but not CD8(+) T cells or CD8-DCs. Our findings suggest that CD8(+) DCs in the lymphoid tissues enable an early step in the development of gamma delta T cells through direct cell contact. DC-expressed CD8 might take part in this interaction.

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  • Plasticity of regulatory T cells: Subversion of suppressive function and conversion to enhancement of lung allergic responses 査読

    Anthony Joetham, Shigeki Matsubara, Masakazu Okamoto, Katsuyuki Takeda, Nobuaki Miyahara, Azzeddine Dakhama, Erwin W. Gelfand

    JOURNAL OF IMMUNOLOGY   180 ( 11 )   7117 - 7124   2008年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Activation of CD4(+)CD25(+)Foxp3(+) naturally occurring regulatory T cells (nTregs) resulting in suppression of lung allergic responses requires interaction of MHC class I on nTregs and CD8. In the absence of CD8 (CD8(-/-) recipients), transferred nTregs restored airway hyperresponsiveness, eosinophilic inflammation, and IL-13 levels following allergen exposure. Enhancement of lung allergic responses was accompanied by reduced expression of Foxp3 and increased expression of IL-13 in the transferred nTregs. In CD8(-/-) recipients pretreated with glucocorticoid-induced TNFR-related protein-ligand Ab, the transferred nTregs maintained high levels of Foxp3 and did not result in altered lung responses. Thus, the regulatory function of nTregs can be subverted by reducing the expression of Foxp3 and following signaling through glucocorticoid-induced TNFR-related protein are converted nTregs into IL-13-producing CD4(+) T cells mediating lung allergic responses.

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  • Estrogen determines sex differences in airway responsiveness after allergen exposure 査読

    Shigeki Matsubara, Christina H. Swasey, Loan E. Loader, Azzeddine Dakhama, Anthony Joetham, Hiroshi Ohnishi, Annette Balhorn, Nobuaki Miyahara, Katsuyuki Takeda, Erwin W. Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   38 ( 5 )   501 - 508   2008年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    The female hormone estrogen is an important factor in the regulation of airway function and inflammation, and sex differences in the prevalence of asthma are well described. Using an animal model, we determined how sex differences may underlie the development of altered airway function in response to allergen exposure. We compared sex differences in the development of airway hyperresponsiveness (AHR) after allergen exposure exclusively via the airways. Ovalbumin (OVA) was administered by nebulization on 10 consecutive days in BALB/c mice. After methacholine challenge, significant AHR developed in male mice but not in female mice. Ovariectomized female mice showed significant AHR after 10-day OVA inhalation. IC11182,780, an estrogen antagonist, similarly enhanced airway responsiveness even when administered 1 hour before assay. In contrast, 17 beta-estradiol dose-dependently suppressed AHR in male mice. In all cases, airway responsiveness was inhibited by the administration of a neurokinin I receptor antagonist. These results demonstrate that sex differences in 10-day OVA-induced AHR are due to endogenous estrogen, which negatively regulates airway responsiveness in female mice. Cumulatively, the results suggest that endogenous estrogen may regulate the neurokinin 1-dependent prejunctional activation of airway smooth muscle in allergen-exposed mice.

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  • 早期に診断し得た肺ランゲルハンス細胞性組織球症の1例

    古賀 光, 谷本 安, 渕本 康子, 大橋 圭明, 宮原 信明, 瀧川 奈義夫, 田端 雅弘, 金廣 有彦, 木浦 勝行, 片岡 幹男, 谷本 光音

    気管支学   30 ( 3 )   160 - 160   2008年5月

  • ゲフィチニブ単剤療法が施行された肺非小細胞癌における予後因子としての血清KL-6

    藤原 義朗, 木浦 勝行, 瀧川 奈義夫, 豊岡 伸一, 堀田 勝幸, 宗 淳一, 宮原 信明, 谷本 安, 金廣 有彦, 田端 雅弘, 加藤 勝也, 伊達 洋至, 谷本 光音

    日本呼吸器学会雑誌   46 ( 増刊 )   131 - 131   2008年5月

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    記述言語:日本語   出版者・発行元:(一社)日本呼吸器学会  

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  • Corticosteroids enhance CD8(+) T cell-mediated airway hyperresponsiveness and allergic inflammation by upregulating leukotriene B-4 receptor 1 査読

    Hiroshi Ohnishi, Nobuaki Miyahara, Azzeddine Dakhama, Katsuyuki Takeda, Steven Mathis, Bodduluri Haribabu, Erwin W. Gelfand

    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY   121 ( 4 )   864 - 871   2008年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY-ELSEVIER  

    Background: Leukotriene B-4 (LTB4) is a potent inflammatory lipid mediator that binds to LTB4 receptor 1 (BLT1). Ligation of BLT1 by LTB4 plays an important role in the recruitment of effector memory CD8(+) T cells into the airways of sensitized and challenged mice.
    Objectives: The effects of the corticosteroid dexamethasone (DEX) on BLT1-expressing effector memory CD8(+) T cells and effector memory CD8(+) T cell-mediated airway hyperresponsiveness (AHR) and allergic inflammation were determined.
    Methods: Effector memory CD8(+) T cells were generated from ovalbumin(257-264)-primed mononuclear cells from OT-1 mice in the presence of IL-2. In some cultures DEX was added. The effects of DEX on BLT1 expression, LTB4-induced Ca2+ influx, phosphorylation of extracellular signal-regulated kinase 1/2, chemotaxis, and effector memory CD8(+) T cell-mediated AHR were examined.
    Results: DEX-treated effector memory CD8(+) T cells showed significant increases in surface expression of BLT1, LTB4-induced intracellular Ca2+ influx, phosphorylation of extracellular signal-regulated kinase 1/2, and chemotaxis. Upregulation of BLT1 by DEX was accompanied by increased IL-2 receptor expression. Adoptive transfer of DEX-treated effector memory CD8(+) T cells into ovalbumin-sensitized and ovalbumin-challenged CD8(-/-) mice resulted in significant increases in AHR, allergic inflammation, goblet cell metaplasia, and numbers of both CD8(+) and CD4(+) T cells in the bronchoalveolar lavage fluid and lungs.
    Conclusions: Corticosteroids upregulate BLT1 on effector memory CD8(+) T cells and related signaling pathways and potentiate allergic airway inflammation and AHR induced by these cells.

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  • Contribution of allergen-specific and nonspecific nasal responses to early-phase and late-phase nasal responses 査読

    Satoko Miyahara, Nobuaki Miyahara, Joseph J. Lucas, Anthony Joetham, Shikegi Matsubara, Hiroshi Ohnishi, Azzeddine Dakhama, Erwin W. Gelfand

    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY   121 ( 3 )   718 - 724   2008年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY-ELSEVIER  

    Background: The relative contributions of the allergen-specific early-phase nasal response and nonspecific nasal response and mast cells to the pathophysiology of allergic rhinitis are not well defined.
    Objectives: To determine the contributions of specific reactivity, nonspecific reactivity, and mast cells to the development of early-phase and late-phase responses using a mouse model of allergic rhinitis.
    Methods: Sensitized wild-type and Fc epsilon RI-deficient (FC epsilon RI(-/-)) mice were exposed to allergen for 3, 5, or 12 days. As indicators of nasal reactivity, respiratory frequency and nasal resistance were monitored.
    Results: Sensitized mice exposed to 3 days of nasal allergen challenge showed a nonspecific early-phase response. As the number of allergen exposures increased, there was progressive diminution in nonspecific responses with increased allergen-specific early-phase responses and a late-phase response. Sensitized Fc epsilon RI(-/-) mice did not develop nonspecific nasal responses or late-phase responses, but transfer of in vitro-differentiated wild-type mast cells into Fc epsilon RI(-/-) mice restored nonspecific early-phase nasal responses but not the late-phase response.
    Conclusion: These data identify the nonspecific nasal response as a major contributor to the early-phase response, especially during initial allergen exposure, and is dependent on mast cells. Increasing allergen exposure results in increasing allergen-specific responses, converting the nonspecific early-phase response to a late-phase response that is allergen-specific and mast cell-independent.

    DOI: 10.1016/j.jaci.2007.11.002

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  • IFN-gamma production during initial infection determines the outcome of reinfection with respiratory syncytial virus 査読

    Young-Mok Lee, Nobuaki Miyahara, Katsuyuki Takeda, John Prpich, Anita Oh, Annette Balhorn, Anthony Joetham, Erwin W. Gelfand, Azzeddine Dakhama

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   177 ( 2 )   208 - 218   2008年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Rationale. Severe respiratory syncytial virus (RSV) bronchiolitis has been associated with deficient IFN-gamma production in humans, but the role of this cytokine in determining the outcome of reinfection is unknown.
    Objectives: To define the role of IFN-gamma in the development of RSV-mediated airway hype rresponsiveness (AHR) and lung histopathology in mice.
    Methods: Wild-type (WT) and IFN-gamma knockout mice were infected with RSV in the newborn or weaning stages and reinfected 5 weeks later. Airway responses were assessed on Day 6 after the primary or secondary infection.
    Measurements and Main Results: Both WT and IFN-gamma knockout mice developed similar levels of AHR and airway inflammation after primary infection. After reinfection, IFN-gamma knockout mice, but not WT mice, developed AHR, airway eosinophilia, and mucus hyperproduction. Intranasal administration of IFN-gamma during primary infection but not during reinfection prevented the development of these altered airway responses on reinfection in IFN-gamma knockout mice. Adoptive transfer of WT T cells into IFN-gamma knockout mice before primary infection restored IFN-gamma production in the lungs and prevented the development of altered airway responses on reinfection. Treatment of mice with IFN-gamma during primary neonatal infection prevented the enhancement of AHR and the development of airway eosinophilia and mucus hyperproduction on reinfection.
    Conclusions: IFN-gamma production during primary RSV infection is critical to the development of protection against AHR and lung histopathology on reinfection. Provision of IFN-gamma during primary infection in infancy may be a potential therapeutic approach to alter the course of RSV-mediated long-term sequelae.

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  • The role of leukotriene B4 in allergic diseases 査読

    Hiroshi Ohnishi, Nobuaki Miyahara, Erwin W. Gelfand

    Allergology International   57 ( 4 )   291 - 298   2008年

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    記述言語:英語   出版者・発行元:Japanese Society of Allergology  

    Leukotriene B4 (LTB4) is a lipid mediator with potent chemoattractant properties and that is rapidly generated from activated innate immune cells such as neutrophils, macrophages, and mast cells. Elevated levels of LTB4 have been reported in various allergic diseases and these levels have been related to disease activity and response to treatment. Recent studies using LTB4 receptor-1 (BLT1) antagonists or BLT1-deficient mice have revealed that ligation of BLT1 by LTB4 is important for the activation and recruitment of inflammatory cells including neutrophils, eosinophils, imonocytes/macrophages, mast cells, dendritic cells, and more recently, effector T cells to inflamed tissues in various inflammatory diseases. The LTB4/BLT1 pathway appears to play an important role in the pathogenesis of severe persistent asthma, aspirin- and exercise-induced asthma, allergic rhinitis, and atopic dermatitis together with other mediators including cysteinyl leukotrienes, cytokines, and chemokines. LTB4 production is in general resistant to corticosteroid treatment. In fact, corticosteroids can upregulate BLT1 expression on corticosteroid-resistant inflammatory cells such as neutrophils, monocytes, and effector memory CD8+ T cells. As a result, this corticosteroid-resistant LTB4/BLT1 pathway may contribute to the development of inflammation in allergic diseases that do not respond to the introduction of corticosteroids. Inhibition of this pathway has potential therapeutic benefit in various allergic diseases that have involvement of corticosteroid-insensitivity. © 2008 Japanese Society of Allergology.

    DOI: 10.2332/allergolint.08-RAI-0019

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  • [Coinfection with Mycoplasma pneumoniae and Chlamydophila pneumoniae in a middle-aged adult]. 査読

    Kubo T, Takigawa N, Tanimoto Y, Ichihara E, Tabata M, Miyahara N, Kanehiro A, Kiura K, Tanimoto M

    Nihon Kokyuki Gakkai zasshi = the journal of the Japanese Respiratory Society   45 ( 10 )   808 - 811   2007年10月

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  • Airway hyperresponsiveness through synergy of gamma delta T cells and NKT cells 査読

    Niyun Jin, Nobuaki Miyahara, Christina L. Roark, Jena D. French, M. Kemal Aydintug, Jennifer L. Matsuda, Laurent Gapin, Rebecca L. O'Brien, Erwin W. Gelfand, Willi K. Born

    JOURNAL OF IMMUNOLOGY   179 ( 5 )   2961 - 2968   2007年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Mice sensitized and challenged with OVA were used to investigate the role of innate T cells in the development of allergic airway hyperresponsiveness (AHR). AHR, but not eosinophilic airway inflammation, was induced in T cell-deficient mice by small numbers of cotransferred gamma(delta) T cells and invariant NKT cells, whereas either cell type alone was not effective. Only V gamma 1(+)V delta 5(+) gamma delta T cells enhanced AHR. Surprisingly, OVA-specific alpha beta T cells were not required, revealing a pathway of AHR development mediated entirely by innate T cells. The data suggest that lymphocytic synergism, which is key to the Ag-specific adaptive immune response, is also intrinsic to T cell-dependent innate responses.

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  • CD8(+) T cell-mediated airway hyperresponsiveness and inflammation is dependent on CD4(+)IL-4(+) T cells 査読

    Toshiyuki Koya, Nobuaki Miyahara, Katsuyuki Takeda, Shigeki Matsubara, Hiroyuki Matsuda, Christina Swasey, Annette Balhorn, Azzeddine Dakhama, Erwin W. Gelfand

    JOURNAL OF IMMUNOLOGY   179 ( 5 )   2787 - 2796   2007年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    CD4(+) T cells, particularly Th2 cells, play a pivotal role in allergic airway inflammation. However, the requirements for interactions between CD4+ and CD8(+) T cells in airway allergic inflammation have not been delineated. Sensitized and challenged OT-1 mice in which CD8(+) T cells expressing the transgene for the OVA(257-264) peptide (SIINFEKL) failed to develop airway hyperresponsiveness (AHR), airway eosinophilia, Th2 cytokine elevation, or goblet cell metaplasia. OT-1 mice that received naive CD4(+)IL-4(+) T cells but not CD4(+)IL-4(-) T cells before sensitization developed all of these responses to the same degree as wild-type mice. Moreover, recipients of CD4(+)IL-4(+) T cells developed significant increases in the number of CD8(+)IL-13(+) T cells in the lung, whereas sensitized OT-1 mice that received primed CD4(+) T cells just before challenge failed to develop these responses. Sensitized CD8-deficient mice that received CD8(+) T cells from OT-1 mice that received naive CD4(+) T cells before sensitization increased AHR and eosinophil numbers in bronchoalveolar lavage fluid when challenged with allergen. In contrast, sensitized CD8-deficient mice receiving CD8(+) T cells from OT-1 mice without CD4(+) T cells developed reduced AHR and eosinophil numbers in bronchoalveolar lavage fluid when challenged. These data suggest that interactions between CD4(+) and CD8(+) T cells, in part through IL-4 during the sensitization phase, are essential to the development of CD8(+)IL-13(+) T cell-dependent AHR and airway allergic inflammation.

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  • Activation of naturally occurring lung CD4(+) CD25(+) regulatory T cells requires CD8 and MHC I interaction 査読

    Anthony Joetham, Katsuyuki Takeda, Nobuaki Miyahara, Shigeki Matsubara, Hiroshi Ohnishi, Toshiyuki Koya, Azzeddine Dakhama, Erwin W. Gelfand

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   104 ( 38 )   15057 - 15062   2007年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATL ACAD SCIENCES  

    Naturally occurring Foxp3(+)CD4(+)CD25(+) T cells (nTregs) isolated from lungs of naive mice regulate allergic airway hyperresponsiveness (AHR) and inflammation. Here, we demonstrate the critical requirement for engagement of MHC class I on CD4(+)CD25(+) T cells by CD8 for the functional activation of these nTregs. Suppression of allergen-induced AHR and inflammation by nTregs was abolished in mice treated with anti-CD8. Correspondingly, decreased levels of IL-10 and TGF-beta and increased levels of Th2 cytokines in bronchoalveolar lavage were detected in these treated mice. Similarly, nTregs isolated from beta 2m(-/-) mice or from mice treated with anti-MHC I antibody in vitro before intratracheal transfer failed to modulate AHR or inflammation. Coculture of nTregs with CD8(+) T cells increased IL-10 and TGF-beta. Addition of anti-MHC I or anti-CD8 reduced IL-10 and TGF-beta. These results demonstrate that functional activation of nTregs requires the interaction between MHC I on CD4(+)CD25(+) T cells and CD8.

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  • 樹状細胞およびロイコトリエンB4受容体のアレルギー性気道反応における役割の検討 査読

    宮原 信明, 松田 宏幸, 宮原 聡子, 大西 広志, 武田 勝行, 岡本 真和, 古賀 光, 渕本 康子, 池田 元洋, 松原 茂樹, 谷本 安, 金廣 有彦, 片岡 幹男, 谷本 光音, Gelfand Erwin W.

    アレルギー   56 ( 8-9 )   1102 - 1102   2007年9月

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    記述言語:日本語   出版者・発行元:(一社)日本アレルギー学会  

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  • Arhgef1 is required by T cells for the development of airway hyperreactivity and inflammation 査読

    Jeanette P. Brown, Christian Taube, Nobuaki Miyahara, Toshiyuki Koya, Roberta Pelanda, Erwin W. Gelfand, Raul M. Torres

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   176 ( 1 )   10 - 19   2007年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Rationale: Arhgef1 is an intracellular protein, expressed by hematopoietic cells, that regulates signaling by both G protein-coupled receptors and RhoA, and, consequently, is required for appropriate migration and adhesion of diverse leukocyte populations. Objectives: To evaluate a possible contribution for Arhgef1 in the development of airway inflammation and airway hyperreactivity. Methods: Arhgef1-deficient (Arhgef1(-/-)) and wild-type (WT) mice were sensitized and airway challenged, followed by measurement of airway responsiveness to inhaled methacholine. Inflammation was assessed by several parameters that included flow cytometric analysis and histology. Arhgef1-deficient recipients were reconstituted with WT T lymphocytes before sensitization and challenge, and again measured for airway responsiveness and inflammation. Cytokine production in response to specific antigen was measured in cultures of isolated leukocytes from lung and spleen and compared with the levels generated in lung and spleen explant cultures. Measurements and Main Results: Arhgef1(-/-) mice display significantly reduced airway hyperreactivity, Th2 cytokine production, and lung inflammation, despite intact systemic immunity. After airway challenge of Arhgef1(-/-) mice, antigen-specific T cells were present in mutant lungs, but were found to interact with CD11c(+) cells at a significantly reduced frequency. Adoptive transfer of WTTcells into Arhgef1(-/-) mice restored airway hyperreactivity and inflammation. Conclusions: These data demonstrate that T cells depend on Arhgef1 to promote lung inflammation. Moreover, a deficiency in Arhgef1 results in reduced T cell-CD11c(+) antigen-presenting cell interaction, and likely underscores the inability of Arhgef1(-/-) mice to mount an adaptive immune response to airway challenge.

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  • IL-10-treated dendritic cells decrease airway hyperresponsiveness and airway inflammation in mice 査読

    Toshiyuki Koya, Hiroyuki Matsuda, Katsuyuki Takeda, Shigeki Matsubara, Nobuaki Miyahara, Annette Balhorn, Azzeddine Dakhama, Erwin W. Gelfand

    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY   119 ( 5 )   1241 - 1250   2007年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY-ELSEVIER  

    Background: IL-10 affects dendritic cell (DC) function, but the effects on airway hyperresponsiveness (AHR) and inflammation are not defined.
    Objective: We sought to determine the importance of IL-10 in regulating DC function in allergen-induced AHR and airway inflammation.
    Methods: DCs were generated from bone marrow in the presence or absence of IL-10. In vivo IL-10-treated DCs from IL-10(+/+) and IL-10(-/-) donors pulsed with ovalbumin (OVA) were transferred to naive or sensitized mice before challenge. In recipient mice AHR, cytokine levels, cell composition of bronchoalveolar lavage (BAL) fluid, and lung histology were monitored.
    Results: In vitro, IL-10-treated DCs expressed lower levels of CD11c, CD80, and CD86; expressed lower levels of IL-12; and suppressed T(H)2 cytokine production. In vivo, after transfer of OVA-pulsed IL-10-treated DCs, naive mice did not have AHR, airway eosinophilia, T(H)2 cytokine increase in BAL fluid, or goblet cell metaplasia when challenged, and in sensitized and challenged mice IL-10-treated I)Cs suppressed these responses. Levels of IL-10 in BAL fluid and numbers of lung CD4(+)IL-10(+) T cells were increased in mice that received OVA-pulsed IL-10-treated DCs. Transfer of IL-10-treated DCs from IL-10-deficient mice were ineffective in suppressing the responses in sensitized and challenged mice.
    Conclusions: These data demonstrate that IL-10-treated DCs are potent suppressors of the development of AHR, inflammation, and T(H)2 cytokine production; these regulatory functions are at least in part through the induction of endogenous (DQ production of IL-10. Clinical implications: Modification of DC function by IL-10 can attenuate lung allergic responses, including the development of AHR.

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  • IL-2 and IL-18 attenuation of airway hyperresponsiveness requires STAT4, IFN-gamma, and natural killer cells 査読

    Shigeki Matsubara, Katsuyuki Takeda, Taku Kodama, Anthony Joetham, Nobuaki Miyahara, Toshiyuki Koya, Christina H. Swasey, Masakazu Okamoto, Azzeddine Dakhama, Erwin W. Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   36 ( 3 )   324 - 332   2007年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    IL-18 is known to induce IFN-gamma production, which is enhanced when combined with IL-2. In the present study, we investigated whether the combination of exogenous IL-2 and IL-18 alters airway hyperresponsiveness (AHR) and airway inflammation. Sensitized mice exposed to ovalbumin (OVA) challenge developed AHR, inflammatory cells in the bronchoalveolar lavage (BAL) fluid, and increases in levels of Th2 cytokines and goblet cell numbers. The combination of IL-2 and IL-18, but neither alone, prevented these changes while increasing levels of IL-12 and IFN-gamma. The combination of IL-2 and IL-18 was ineffective in IFN-gamma-deficient and signal transducer and activator of transcription (STAT)4-deficient mice. Flow cytometry analysis showed significant increases in numbers of IFN-gamma-positive natural killer (NK) cells in the lung after treatment with the combination therapy, and transfer of lung NK cells isolated from sensitized and challenged mice treated with the combination significantly suppressed AHR and BAL eosinophilia. These data demonstrate that the combination of IL-2 and IL-18 prevents AHR and airway inflammation, likely through IL-12-mediated induction of IFN-gamma production in NK cells.

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  • Naturally occurring lung CD4(+) CD25(+) T cell regulation of airway allergic responses depends on IL-10 induction of TGF-beta 査読

    Anthony Joetham, Katsuyuki Takada, Christian Taube, Nobuaki Miyahara, Satoko Matsubara, Toshiyuki Koya, Yeong-Ho Rha, Azzeddine Dakhama, Erwin W. Gelfand

    JOURNAL OF IMMUNOLOGY   178 ( 3 )   1433 - 1442   2007年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Peripheral tolerance to allergens is mediated in large part by the naturally occurring lung CD4(+)CD25(+) T cells, but their effects on allergen-induced airway responsiveness have not been well defined. Intratracheal, but not i.v., administration of naive lung CD4(+)CD25(+) T cells before allergen challenge of sensitized mice, similar to the administration of the combination of rIL-10 and rTGF-beta, resulted in reduced airway hyperresponsiveness (AHR) and inflammation, lower levels of Th2 cytokines, higher levels of IL-10 and TGF-beta, and less severe lung histopathology. Significantly, CD4(+)CD25(+) T cells isolated from IL-10(-/-) mice had no effect on AHR and inflammation, but when incubated with rIL-10 before transfer, suppressed AHR, and inflammation, and was associated with elevated levels of bronchoalveolar lavage TGF-beta levels. By analogy, anti-TGF-beta treatment reduced regulatory T cell activity. These data identify naturally occurring lung CD4(+)CD25(+) T cells as capable of regulating lung allergic responses in an IL-10- and TGF-beta-dependent manner.

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  • Critical role of the Fc receptor gamma-chain on APCs in the development of allergen-induced airway hyperresponsiveness and inflammation 査読

    Kenichi Kitamura, Katsuyuki Takeda, Toshiyuki Koya, Nobuaki Miyahara, Taku Kodama, Azzeddine Dakhama, Toshiyuki Takai, Atsushi Hirano, Mitsune Tanimoto, Mine Harada, Erwin W. Gelfand

    JOURNAL OF IMMUNOLOGY   178 ( 1 )   480 - 488   2007年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    The FeR common y-chain (FcRy) is an essential component of the receptors Fe epsilon RI, Fc gamma RI, and Fc gamma RIII, which are expressed on many inflammatory cell types. The role of these receptors in the initiation or maintenance of allergic inflammation has not been well defined. FcR gamma-deficient (FcRy(-/-)) and control (wild-type (WT)), mice were sensitized and subsequently challenged with OVA. Following sensitization and challenge to OVA, FeRy-deficient (FcRy(-/-)) mice developed comparable levels of IgE and IgG1 as WT mice. However, numbers of eosinophils, levels of IL-5, IL-13, and eotaxin in bronchoalveolar lavage fluid, and mononuclear cell (MNC) proliferative responses to OVA were significantly reduced, as was airway hyperresponsiveness (AHR) to inhaled methacholine. Reconstitution of FeRy(-/-) mice with whole spleen MNC from WT mice before sensitization restored development of AHR and the numbers of eosinophils in bronchoalveolar lavage fluid; reconstitution after sensitization but before OVA challenge only partially restored these responses. These responses were also restored when FcRy(-/-) mice received T cell-depleted MNC, T and B cell-depleted MNC, or bone marrow-derived dendritic cells before sensitization from FcR(+/+) or Fe gamma RIII-deficient but not FcRy(-/-) mice. The expression levels of Fc gamma RIV on bone marrow-derived dendritic cells from FcR(+/+) mice were found to be low. These results demonstrate that expression of FcR gamma, most likely Fc gamma RI, on APCs is important during the sensitization phase for the development of allergic airway inflammation and AHR.

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  • IL-13 is essential to the late-phase response in allergic rhinitis 査読

    Satoko Miyahara, Nobuaki Miyahara, Shigeki Matsubara, Katsuyuki Takeda, Toshiyuki Koya, Erwin W. Gelfand

    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY   118 ( 5 )   1110 - 1116   2006年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY-ELSEVIER  

    Background: The pathophysiology of the early- and late-phase nasal response to allergen challenge is not completely defined. Recent technical advances enable direct monitoring of these responses in mice.
    Objective: IL-13 is detected in the nasal membranes of both human beings and mice with allergic rhinitis, but its role in disease pathogenesis is unclear. We measured early and late nasal allergic responses after treatment with soluble IL-13R alpha 2-IgG fusion protein (sIL-13R alpha 2-Fc), and in IL-13-deficient mice (IL-13(-/-)).
    Methods: IL-13(-/-) mice (BALB/c background) and wild-type mice were sensitized to ovalbumin by intraperitoneal injection and then challenged intranasally with ovalbumin without sedation. The sIL-13R alpha 2-Fc or control human IgG was administered by intraperitoneal (i.p.) injection 24 hours and 1 hour before each ovalbumin challenge. Early nasal responses after the 4th ovalbumin challenge and late nasal responses 24 hours after the 6th ovalbumin challenge were assessed. Results: Sensitized/challenged wild-type mice treated with sIL-13R alpha 2-Fc or IL-13(-/-) mice demonstrated significantly reduced late nasal responses in face of persistent nasal tissue eosinophilia; the early nasal response was little affected by targeting IL-13. Goblet cell hyperplasia was not detected in nasal membranes.
    Conclusion: The data indicate that IL-13 is a major contributor to the development of a late nasal response with little influence on the early response, and without affecting nasal eosinophilic inflammation. Inhibition of IL-13 may have an important therapeutic application in preventing the persistent nasal blockage in allergic rhinitis.
    Clinical implications: Current therapies for allergic rhinitis may not take into account the important differences in the pathophysiology of the early and late responses and the important role of IL-13 in sustaining chronic nasal congestion and obstruction.

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  • RANTES (CCL5) regulates airway responsiveness after repeated allergen challenge 査読

    Toshiyuki Koya, Katsuyuki Takeda, Taku Kodama, Nobuaki Miyahara, Shigeki Matsubara, Annette Balhorn, Anthony Joetham, Azzedine Dakhama, Erwin W. Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   35 ( 2 )   147 - 154   2006年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    RANTES (CC chemokine ligand 5) contributes to airway inflammation through accumulation of eosinophils, but the exact role of RANTES (CCL5) is not defined. C57BL/6 mice, sensitized by injection of ovalbumin (OVA) on Days I and 14, were challenged with OVA on Days 28, 29, and 30 (3 challenges, short-term-challenge model) or on Days 28, 29, 30, 36, 40, 44, and 48 (7 challenges, repeated-challenge model) and evaluated 48 h later. Anti-mouse RANTES was given intravenously, and recombinant mouse RANTES or PBS was given intratracheally. These reagents were given on Days 28, 29, and 30 in the short-term-challenge study and on Days 44 and 48 in the repeated-challenge study. After short-term challenge, there were no effects after administration of anti-RANTES or RANTES. In the repeated-challenge study, although control mice showed a decrease in airway hyperresponsiveness, administration of anti-RANTES sustained and enhanced airway hyperresponsiveness and increased goblet cell numbers. In contrast, administration of RANTES normalized airway function but reduced goblet cell numbers. IL-12 and IFN-gamma levels in BAL decreased in the anti-RANTES group and increased in the RANTES group. IFN-gamma-producing CD4 T cells in lung, and IFN-gamma production from lung T cells in response to OVA in the anti-RANTES group, were significantly decreased but were increased in the RANTES group. Anti-IFN-gamma administered with RANTES, decreased the effects of RANTES on AHR after repeated challenge. These data indicate that RANTES plays a role in the regulation of airway function after repeated allergen challenge, in part through modulation of levels of IFN-gamma and IL-12.

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  • Role of the LTB4/BLT1 pathway in allergen-induced airway hyperresponsiveness and inflammation. 査読

    Miyahara N, Miyahara S, Takeda K, Gelfand EW

    Allergology international : official journal of the Japanese Society of Allergology   55 ( 2 )   91 - 97   2006年6月

  • Factor B of the alternative complement pathway regulates development of airway hyperresponsiveness and inflammation 査読

    C Taube, JM Thurman, K Takeda, A Joetham, N Miyahara, MC Carroll, A Dakhama, PC Giclas, VM Holers, EW Gelfand

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   103 ( 21 )   8084 - 8089   2006年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATL ACAD SCIENCES  

    Exposure to inhaled allergens leads to increases in airway hyper-responsiveness (AHR) and inflammation, associated with increased levels of biologically active fragments derived from the complement C3 and C5 family of proteins. Further, complement activation during allergen challenge in sensitized animals is necessary for the development of AHR and airway inflammation. To define the complement pathway involved, we studied mice deficient in complement factor 4 (C4-/-), a critical component of the classical pathway, or factor B (fB-/-), an essential protein in the alternative complement pathway. WT, C4-/-, and fB-/- mice were sensitized to ovalbumin and subsequently exposed to nebulized ovalbumin (1% in saline) on 3 consecutive days. After allergen sensitization and challenge, fB-/- mice demonstrated significantly lower airway responsiveness to methacholine and less airway inflammation. In contrast, C4-/- mice showed no reduction in AHR and airway inflammation compared with WT mice. Tissue inflammation, goblet cell hyperplasia, and IL-4, IL-5, and IL-13 levels in BAL fluid were significantly reduced in fB-/- mice compared with C4-/- and WT mice. The development of AHR and airway inflammation in sensitized fB-/- mice could be restored after intranasal administration of purified factor B before the airway challenge. In addition, administration of a neutralizing anti-factor B mAb to sensitized mice before airway challenge reduced the development of AHR and airway inflammation. These results demonstrate that in sensitized hosts complement activation through the alternative pathway after allergen exposure is critical to the development of AHR and airway inflammation.

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  • Syk activation in dendritic cells is essential for airway hyperresponsiveness and inflammation 査読

    S Matsubara, T Koya, K Takeda, A Joetham, N Miyahara, P Pine, ES Masuda, CH Swasey, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   34 ( 4 )   426 - 433   2006年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    We evaluated the role of Syk, using an inhibitor, on allergen-induced airway hyperresponsiveness (AHR) and airway inflammation in a system shown to be B cell- and mast cell-independent. Sensitization of BALB/c mice with ovalbumin (OVA) and alum after three consecutive OVA challenges resulted in AHR to inhaled methacholine and airway inflammation. The Syk inhibitor R406 (30 mg/kg, administered orally, twice daily) prevented the development of AHR, increases in eosinophils and lymphocytes and IL-13 levels in bronchoalveolar lavage (BAL) fluid, and goblet cell metaplasia when administered after sensitization and before challenge with OVA. Levels of IL-4, IL-5, and IFN-gamma in BAL fluid and allergen-specific antibody levels in serum were not affected by treatment. Because many of these responses may be influenced by dendritic cell function, we investigated the effect of R406 on bone marrow-derived dendritic cell (BMDC) function. Co-culture of BMDC with immune complexes of OVA and IgG anti-OVA together with OVA-sensitized spleen mononuclear cells resulted in increases in IL-13 production. IL-13 production was inhibited if the BMDCs were pretreated with the Syk inhibitor. Intratracheal transfer of immune complex-pulsed BMDCs (but not nonpulsed BMDCs) to naive mice before airway allergen challenge induced the development of AHR and increases in BAL eosinophils and lymphocytes. All of these responses were inhibited if the transferred BMDCs were pretreated with R406. These results demonstrate that Syk inhibition prevents allergen-induced AHR and airway inflammation after systemic sensitization and challenge, at least in part through alteration of DC function.

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  • The leukotriene B4 receptor (BLT1) is required for effector CD8(+) T cell-mediated, mast cell-dependent airway hyperresponsiveness 査読

    C Taube, N Miyahara, Ott, V, B Swanson, K Takeda, J Loader, LD Shultz, AM Tager, AD Luster, A Dakhama, EW Gelfand

    JOURNAL OF IMMUNOLOGY   176 ( 5 )   3157 - 3164   2006年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Studies in both humans and rodents have suggested that CD8(+) T cells contribute to the development of airway hyperresponsiveness (AHR) and that leukotriene B4 (LTB4) is involved in the chemotaxis of effector CD8(+) T cells (T-EFF) to the lung by virtue of their expression of BLT1, the receptor for LTB4. In the present study, we used a mast cell-CD8-dependent model of AHR to further define the role of BLT1 in CD8(+) T cell-mediated AHR. C57BL/6(+/+) and CD8-deficient (CD8(-/-)) mice were passively sensitized with anti-OVA IgE and exposed to OVA via the airways. Following passive sensitization and allergen exposure, C57BL/6(+/+) mice developed altered airway function, whereas passively sensitized and allergen-exposed CD8(-/-) mice failed to do so. CD8(-/-) mice reconstituted with CD8(+) T-EFF developed AHR in response to challenge. In contrast, CD8(-/-) mice reconstituted with BLT1-deficient effector CD8(+) T cells did not develop AHR. The induction of increased airway responsiveness following transfer of CD8(+) TEFF or in wild-type mice could be blocked by administration of an LTB4 receptor antagonist confirming the role of BLT1 in CD8(+) T cell-mediated AHR. Together, these data define the important role for mast cells and the LTB4-BLT1 pathway in the development of CD8(+) T cell-mediated allergic responses in the lung.

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  • Importance of myeloid dendritic cells in persistent airway disease after repeated allergen exposure 査読

    T Koya, T Kodama, K Takeda, N Miyahara, ES Yang, C Taube, A Joetham, JW Park, A Dakhama, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   173 ( 1 )   42 - 55   2006年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Rationale: There is conflicting information about the development and resolution of airway inflammation and airway hyperresponsiveness (AHR) after repeated airway exposure to allergen in sensitized mice.
    Methods: Sensitized BALB/c and C57BL/6 mice were exposed to repeated allergen challenge on 3, 7, or I I occasions. Airway function in response to inhaled methacholine was monitored; bronchoalveolar lavage fluid inflammatory cells were counted; and goblet cell metaplasia, peribronchial fibrosis, and smooth muscle hypertrophy were quantitated on tissue sections. Bone marrow-derived dendritic cells were generated after differentiation of bone marrow cells in the presence of growth factors.
    Results: Sensitization to ovalbumin (OVA) in alum, followed by three airway exposures to OVA, induced lung eosinophilia, goblet cell metaplasia, mild peribronchial fibrosis, and peribronchial smooth muscle hypertrophy; increased levels of interleukin (IL)-4, IL-5, IL-13, granulocyte-macrophage colony-stimulating factor, transforming growth factor-beta(1), eotaxin-1, RANTES (regulated on activation, normal T-cell expressed and secreted), and OVA-specific IgG1 and IgE; and resulted in AHR. After seven airway challenges, development of AHR was markedly decreased as was the production of IL-4, IL-5. and IL-13. Levels of IL-10 in both strains and the level of IL-12 in BALB/c mice increased. After 11 challenges, airway eosinophilia and peribronchial fibrosis further declined and the cytokine and chemokine profiles continued to change. At this time point, the number of myeloid dendritic cells and expression of CD80 and CD86 in lungs were decreased compared with three challenges. After 11 challenges, intratracheal instillation of bone marrow-derived dendritic cells restored AHR and airway eosinophilia.
    Conclusions: These data suggest that repeated allergen exposure leads to progressive decreases in AHR and allergic inflammation, through decreases in myeloid dendritic cell numbers.

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  • Inhibition of spleen tyrosine kinase prevents mast cell activation and airway hyperresponsiveness 査読

    S Matsubara, GM Li, K Takeda, JE Loader, P Pine, ES Masuda, N Miyahara, S Miyahara, JJ Lucas, A Dakhama, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   173 ( 1 )   56 - 63   2006年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Rationale: Spleen tyrosine kinase (Syk) is important for Fc and B-cell receptor-mediated signaling.
    Objective: To determine the activity of a specific Syk inhibitor (11406) on mast cell activation in vitro and on the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation in vivo.
    Methods: AHR and inflammation were induced after 10 d of allergen (ovalbumin [OVA]) exposure exclusively via the airways and in the absence of adjuvant. This approach was previously established to be IgE, Fc epsilon RI, and mast cell dependent. Alternatively, mice were passively sensitized with OVA-specific IgE, followed by limited airway challenge. In vitro, the inhibitor was added to cultures of IgE-sensitized bone marrow-derived mast cells (BMMCs) before crosslinking with allergen.
    Results: The inhibitor prevented OVA-induced degranulation of passively IgE-sensitized murine IBMMCs and inhibited the production of interieukin (IL)-13, tumor necrosis factor a, IL-2, and IL-6 in these sensitized BMMCs. When administered in vivo, R406 inhibited AHR, which developed in BALB/c mice exposed to aerosolized 1% OVA for 10 consecutive d (20 min/d), as well as pulmonary eosinophilia and goblet cell metaplasia. A similar inhibition of AHR was demonstrated in mice passively sensitized with OVA-specific IgE and exposed to limited airway challenge.
    Conclusion: This study delineates a functional role for Syk in the development of mast cell- and IgE-mediated AHR and airway inflammation, and these results indicate that inhibition of Syk may be a target in the treatment of allergic asthma.

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  • Physiologic assessment of allergic rhinitis in mice: Role of the high-affinity IgE receptor (Fc epsilon RI) 査読

    S Miyahara, N Miyahara, K Takeda, A Joetham, EW Gelfand

    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY   116 ( 5 )   1020 - 1027   2005年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY, INC  

    Background: There have been few reports using animal models to study the development of allergic rhinitis. Characterization of such a model in mice would be advantageous given the availability of reagents and gene-manipulated strains.
    Objective: We sought to develop a murine model of allergic rhinitis in the absence of lower airway changes.
    Methods: After sensitization and challenge, both wild-type and Fe epsilon RI-deficient mice were studied for their ability to develop early- and late-phase nasal responses. In the invasive approach, direct measurements of nasal airway resistance (R-NA) were obtained; in the noninvasive approach using whole-body plethysmography, respiratory frequency and expiratory and inspiratory times were monitored. In both approaches, nasal responses were determined either acutely after challenge (early phase) or 24 hours after challenge (late phase).
    Results: After challenge of sensitized mice, R-NA significantly increased. In parallel, respiratory frequency significantly decreased and was highly correlated with the increases in R-NA-Sensitized wild-type mice had an early-phase nasal response and persistent nasal blockage (late-phase response) after allergen challenge. In contrast, sensitized and challenged Fc epsilon RI alpha-chain-deficient mice did not have an early-phase nasal reaction and exhibited reduced nasal blockage and lower IL-13 levels in nasal tissue homogenates.
    Conclusions: These data indicate that Fc epsilon RI is essential to development of an early-phase nasal response and contributes to the development of the late-phase nasal response. These invasive and noninvasive approaches provide new opportunities to evaluate the mechanisms underlying the development of nasal responses to allergen and to assess various therapeutic interventions.

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  • S-carboxymethylcysteine normalises airway responsiveness in sensitised and challenged mice 査読

    K Takeda, N Miyahara, T Kodama, C Taube, A Balhorn, A Dakhama, K Kitamura, A Hirano, M Tanimoto, EW Gelfand

    EUROPEAN RESPIRATORY JOURNAL   26 ( 4 )   577 - 585   2005年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:EUROPEAN RESPIRATORY SOC JOURNALS LTD  

    S-carboxymethylcysteine (S-CMC) has been used as a mucoregulator in respiratory diseases. However, the mechanism of action of S-CMC on allergic airway inflammation has not yet been defined.
    In the present study, BALB/c mice were initially sensitised and challenged to ovalbumin (OVA) and, weeks later, re-challenged with OVA (secondary challenge). S-CMC (5-100 mg.kg(-1)) was administered from 2 days before the secondary challenge through to the day of assay.
    Mice developed airway hyperresponsiveness (AHR) 6 h after the secondary challenge and increased numbers of neutrophils were present in the bronchoalveolar lavage (BAL) fluid. At 72 h after secondary challenge, mice again developed AHR, but the BAL fluid contained large numbers of eosinophils. S-CMC treatment was found to reduce AHR and neutrophilia at 6 h, as well as eosinophilia and AHR at 72 h. These effects appeared to be dose dependent. Goblet cell hyperplasia, observed at 72 h, was reduced by S-CMC. In BAL fluid, increased levels of interferon-gamma, interleukin (IL)-12 and IL-10 and decreased levels of IL-5 and IL-13 were detected.
    In conclusion, the data indicate that S-carboxymethylcysteine is effective in reducing airway hyperresponsiveness and airway inflammation at two distinct phases of the response to the secondary allergen challenge in sensitised mice.

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  • The enhancement or prevention of airway hyperresponsiveness during reinfection with respiratory syncytial virus is critically dependent on the age at first infection and IL-13 production 査読

    A Dakhama, JW Park, C Taube, A Joetham, A Balhorn, N Miyahara, K Takeda, EW Gelfand

    JOURNAL OF IMMUNOLOGY   175 ( 3 )   1876 - 1883   2005年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Respiratory syncytial virus (RSV) infection in early life is suspected to play a role in the development of postbronchiolitis wheezing and asthma. Reinfection is common at all ages, but factors that determine the development of altered airway function after reinfection are not well understood. This study was conducted in a mouse model to define the role of age in determining the consequences on airway function after reinfection. Mice were infected shortly after birth or at weaning and were reinfected 5 wk later, followed by assessment of airway function, airway inflammation, and lung histopathology. Infection of mice at weaning elicited a protective airway response upon reinfection. In this age group, reinfection resulted in increased airway inflammation, but without development of airway hyperresponsiveness (AHR) or eosinophilia and decreased IL-13 levels. By contrast, neonatal infection failed to protect the airways and resulted in enhanced AHR after reinfection. This secondary response was associated with the development of airway eosinophilia, increased IL-13 levels, and mucus hyperproduction. Both CD4- and CD8-positive T cells were a source of IL-13 in the lung, and inhibition of IL-13 abolished AHR and mucus production in these mice. Inoculation of UV-inactivated virus failed to elicit these divergent responses to reinfection, emphasizing the requirement for active lung infection during initial exposure. Thus, neonatal RSV infection predisposes to the development of airway eosinophilia and enhanced AHR via an IL-13-dependent mechanism during reinfection, whereas infection at a later age protects against the development of these altered airway responses after reinfection.

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  • Requirement for leukotriene B-4 receptor 1 in allergen-induced airway hyperresponsiveness 査読

    N Miyahara, K Takeda, S Miyahara, S Matsubara, T Koya, A Joetham, E Krishnan, A Dakhama, B Haribabu, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   172 ( 2 )   161 - 167   2005年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Rationale: Leukotriene B-4 (LTB4) is a rapidly synthesized, early leukocyte chemoattractant that signals via its cell surface receptor, leukotriene B4 receptor 1 (BLT1), to attract and activate leukocytes during inflammation. A role for the LTB4-BLT1 pathway in allergen-induced airway hyperresponsiveness and inflammation is not well defined. Objectives: To define the role of the LTB4 receptor (BLT1) in the development of airway inflammation and altered airway function. Methods: BLT1-deficient (BLT1(-/-)) mice and wild-type mice were sensitized to ovalbumin by intraperitoneal injection and then challenged with ovalbumin via the airways. Airway responsiveness to inhaled methacholine, bronchoalveolar lavage fluid cell composition and cytokine levels, and lung inflammation and goblet cell hyperplasia were assessed. Results: Compared with wild-type mice, BLT1(-/-) mice developed significantly lower airway responsiveness to inhaled methacholine, lower goblet cell hyperplasia in the airways, and decreased interleukin (IL)-13 production both in vivo, in the bronchoalveolar lavage fluid, and in vitro, after antigen stimulation of lung cells in culture. Intracellular cytokine staining of lung cells revealed that bronchoalveolar lavage IL-1 3 levels and numbers of IL-13(+)/CD4(+) and IL-13(+)/CD8(+) T cells were also reduced in BLT1 (-/-) mice. Reconstitution of sensitized and challenged BLT1(-/-) mice with allergen-sensitized BLT1(+/+) T cells fully restored the development of airway hyperresponsiveness. In contrast, transfer of naive T cells failed to do so. Conclusion: These data suggest that BLT1 expression on primed T cells is required for the full development of airway hyperresponsiveness, which appears to be associated with IL-13 production in these cells.

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  • Airway hyperresponsiveness in the absence of CD4+T cells after primary but not secondary challenge 査読

    A Joetham, K Takeda, C Taube, N Miyahara, A Kanehiro, A Dakhama, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   33 ( 1 )   89 - 96   2005年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    CD4+ T cells have been shown to play a role in the development of airway hyperresponsivness (AHR) and airway eosinophilia in mice using ablation as well as adoptive transfer experiments. However, as other T cell subsets (CD8, NKT) may play a role in these models, we examined the responses of sensitized CD4-deficient mice after either primary or secondary airway allergen challenge. After sensitization, CD4-deficiency in mice was not associated with airway eosinophilia, allergen-specific IgE, or elevated levels of interleukin (IL)-4 or IL-13. Increases in lung CD8 T cells and IL-5 were observed and shown to be essential for AHR as demonstrated after CD8 T cell depletion or anti-IL-5 treatment. In contrast to the response of sensitized CD4-deficient mice to primary allergen challenge, they failed to develop AHR after secondary allergen challenge. Although the importance of this CD4+ T cell-independent pathway in normal mice is unclear at this time, these studies identify the diversity of the cellular pathway, which may contribute to the development of AHR after primary allergen exposure of sensitized mice.

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  • Leukotriene B4 receptor-1 is essential for allergen-mediated recruitment of CD8(+) T cells and airway hyperresponsiveness 査読

    N Miyahara, K Takeda, S Miyahara, C Taube, A Joetham, T Koya, S Matsubara, A Dakhama, AM Tager, AD Luster, EW Gelfand

    JOURNAL OF IMMUNOLOGY   174 ( 8 )   4979 - 4984   2005年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Recent studies in both human and rodents have indicated that in addition to CD4(+) T cells, CD8(+) T cells play an important role in allergic inflammation. We previously demonstrated that allergen-sensitized and -challenged CD8-deficient (CD8(-/-)) mice develop significantly lower airway hyperresponsiveness (AHR), eosinophilic inflammation, and IL-13 levels in bronchoalveolar lavage fluid compared with wild-type mice, and that all these responses were restored by adoptive transfer of in vivo-primed CD8(+) T cells or in vitro-generated effector CD8(+) T cells (T-EFF). Recently, leukotriene B4 and its high affinity receptor, BLT1, have been shown to mediate in vitro-generated T-EEF recruitment into inflamed tissues. In this study we investigated whether BLT1 is essential for the development of CD8(+) T cell-mediated allergic AHR and inflammation. Adoptive trans fer of in vivo-primed BLT1(+/+), but not BLTI-/-, CD8(+) T cells into sensitized and challenged CD8(-/-) mice restored AHR, eosinophilic inflammation, and IL-13 levels. Moreover, when adoptively transferred into sensitized CD8(-/-) mice, in vitro-generated BLTI+/+, but not BLT1(-/-), T-EFF accumulated in the lung and mediated these altered airway responses to allergen challenge. These data are the first to show both a functional and an essential role for BLT1 in allergen-mediated CD8(+) T-EFF recruitment into the lung and development of AHR and airway inflammation.

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  • Alteration of airway neuropeptide expression and development of airway hyperresponsiveness following respiratory syncytial virus infection 査読

    A Dakhama, JW Park, C Taube, M El Gazzar, T Kodama, N Miyahara, K Takeda, A Kanehiro, A Balhorn, A Joetham, JE Loader, GL Larsen, EW Gelfand

    AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY   288 ( 4 )   L761 - L770   2005年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    The mechanisms by which respiratory syncytial virus (RSV) infection causes airway hyperresponsiveness (AHR) are not fully established. We hypothesized that RSV infection may alter the expression of airway sensory neuropeptides, thereby contributing to the development of altered airway function. BALB/c mice were infected with RSV followed by assessment of airway function, inflammation, and sensory neuropeptide expression. After RSV infection, mice developed significant airway inflammation associated with increased airway resistance to inhaled methacholine and increased tracheal smooth muscle responsiveness to electrical field stimulation. In these animals, substance P expression was markedly increased, whereas calcitonin gene-related peptide ( CGRP) expression was decreased in airway tissue. Prophylactic treatment with Sendide, a highly selective antagonist of the neurokinin-1 receptor, or CGRP, but not the CGRP antagonist CGRP( 8 - 37), inhibited the development of airway inflammation and AHR in RSV-infected animals. Therapeutic treatment with CGRP, but not CGRP( 8 - 37) or Sendide, abolished AHR in RSV-infected animals despite increased substance P levels and previously established airway inflammation. These data suggest that RSV-induced airway dysfunction is, at least in part, due to an imbalance in sensory neuropeptide expression in the airways. Restoration of this balance may be beneficial for the treatment of RSV-mediated airway dysfunction.

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  • The role of virus-specific immunoglobulin E in airway hyperresponsiveness 査読

    A Dakhama, JW Park, C Taube, K Chayama, A Balhorn, A Joetham, XD Wei, RH Fan, C Swasey, N Miyahara, T Kodama, A Alvarez, K Takeda, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   170 ( 9 )   952 - 959   2004年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    Respiratory syncytial virus (RSV) is the most common cause of bronchiolitis during infancy and is associated with subsequent wheezing and asthma, but the nature of this association is not fully understood. We investigated the role of RSV-specific IgE antibodies in the pathophysiology of virus-induced airway dysfunction in a mouse model. Lung infection with RSV resulted in significant increases in mRNA expression for IgE and both of its high- and low-affinity receptors. In serum, virus-specific IgE antibodies reached peak levels by Day 21 after infection. Data from in vitro experiments show that RSV can induce mast cell degranulation, but only if these cells are sensitized with specific IgE. When passively sensitized in vivo with virus-specific IgE, mice developed exaggerated airway responsiveness to methacholine on airway infection, an effect that required the high-affinity receptor of IgE. These data suggest that RSV-specific IgE may contribute to the pathophysiology of airway dysfunction in children who develop this class of specific antibody.

    DOI: 10.1164/rccm.200311-1610oc

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  • Effector CD8(+) T cells mediate inflammation and airway hyper-responsiveness 査読

    N Miyahara, BJ Swanson, K Takeda, C Taube, S Miyahara, T Kodama, A Dakhama, VL Ott, EW Gelfand

    NATURE MEDICINE   10 ( 8 )   865 - 869   2004年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATURE PUBLISHING GROUP  

    Allergic asthma is a complex syndrome characterized by airway obstruction, airway inflammation and airway hyperresponsiveness (AHR). Using a mouse model of allergen-induced AHR, we previously demonstrated that CD8-deficient mice develop significantly lower AHR, eosinophilic inflammation and interleukin (IL)-13 levels in bronchoalveolar lavage fluid compared with wild-type mice. These responses were restored by adoptive transfer of antigen-primed CD8(+) T cells(1). Previously, two distinct populations of antigen-experienced CD8(+) T cells, termed effector (T-EFF) and central memory (T-CM) cells, have been described(2-5). After adoptive transfer into CD8-deficient mice, T-EFF, but not T-CM, cells restored AHR, eosinophilic inflammation and IL-13 levels. T-EFF, but not T-CM, cells accumulated in the lungs, and intracellular cytokine staining showed that the transferred T-EFF cells were a source of IL-13. These data suggest an important role for effector CD8(+) T cells in the development of AHR and airway inflammation, which may be associated with their Tc2-type cytokine production and their capacity to migrate into the lung.

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  • Interleukin-1 receptor antagonist attenuates airway hyperresponsiveness following exposure to ozone 査読

    JW Park, C Taube, C Swasey, T Kodama, A Joetham, A Balhorn, K Takeda, N Miyahara, CB Allen, A Dakhama, SH Kim, CA Dinarello, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY   30 ( 6 )   830 - 836   2004年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    The role of an interleukin (IL)-1 receptor antagonist (IL-1Ra) on the development of airway hyperresponsiveness (AHR) and airway inflammation following acute O-3 exposure in mice was investigated. Exposure of C57/BL6 mice to O-3 at a concentration of 2.0 ppm or filtered air for 3 h resulted in increases in airway responsiveness to inhaled methacholine (MCh) 8 and 16 h after the exposure, and an increase in neutrophils in the bronchoalveolar lavage (BAL) fluid. IL-1beta expression, assessed by gene microarray, was increased 2-fold 4 h after O-3 exposure, and returned to baseline levels by 24 h. Levels of IL-1beta in lung homogenates were also increased 8 h after O-3 exposure. Administration of (human) IL-1Ra before, and after O-3 exposure prevented development of AHR and decreased BAL fluid neutrophilia. Increases in chemokine levels in lung homogenates, tumor necrosis factor-alpha, MIP-2, and keratinocyte chemoattractant following O-3 exposure were prevented by IL-1Ra. Inhalation of dexamethasone, an inhibitor of IL-1 production, blocked the development of AHR, BAL fluid neutrophilia, and decreased levels of IL-1 following O-3 exposure. In summary, acute exposure to O-3 induces AHR, neutrophilic inflammation, epithelial damage, and IL-1. An IL-1Ra effectively prevents the development of altered airway function, inflammation, and structural damage.

    DOI: 10.1165/rcmb.2003.0373OC

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  • Mast cells, Fc epsilon RI, and IL-13 are required for development of airway hyperresponsiveness after aerosolized allergen exposure in the absence of adjuvant 査読

    C Taube, XD Wei, CH Swasey, A Joetham, S Zarini, T Lively, K Takeda, J Loader, N Miyahara, T Kodama, LD Shultz, DD Donaldson, EH Hamelmann, A Dakhama, EW Gelfand

    JOURNAL OF IMMUNOLOGY   172 ( 10 )   6398 - 6406   2004年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    In certain models of allergic airway disease, mast cells facilitate the development of inflammation and airway hyper-responsiveness (AHR). To define the role of the high affinity IgE receptor (Fcis an element ofRI) in the development of AHR, mice with a disruption of the a subunit of the high affinity IgE receptor (Fcis an element ofRI(-/-)) were exposed on 10 consecutive days to nebulized OVA. Forty-eight hours after the last nebulization, airway responsiveness was monitored by the contractile response of tracheal smooth muscle to electrical field. stimulation (EFS). After the 10-day OVA challenge protocol, wild-type mice demonstrated increased responsiveness to EFS, whereas similarly challenged Fcis an element ofRI(-/-) mice showed a low response to EFS, similar to nonexposed animals. Further, allergen-challenged Fcis an element ofRI(-/-) mice showed less airway inflammation, goblet cell hyperplasia, and lower levels of IL-13 in lung homogenates compared with the controls. IL-13-deficient mice failed to develop an increased response to EFS or goblet cell hyperplasia after the 10-day OVA challenge. We transferred bone marrow-derived mast cells from wild-type mice to Fcis an element ofRI(-/-) mice 1 day before initiating the challenge protocol. After the 10-day OVA challenge, recipient Fcis an element ofRI(-/-) mice demonstrated EFS-induced responses similar to those of challenged wild-type mice. Transferred mast cells could be detected in tracheal preparations. These results show that Fcis an element ofRI is important for the development of AHR after an aerosolized allergen sensitization protocol and that this effect is mediated through Fcis an element ofRI on mast cells and production of IL-13 in the lung.

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  • Contribution of antigen-primed CD8(+) T cells to the development of airway hyperresponsiveness and inflammation is associated with IL-13 査読

    N Miyahara, K Takeda, T Kodama, A Joetham, C Taube, JW Park, S Miyahara, A Balhorn, A Dakhama, EW Gelfand

    JOURNAL OF IMMUNOLOGY   172 ( 4 )   2549 - 2558   2004年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    The role of Th2/CD4 T cells, which secrete IL-4, IL-5, and IL-13, in allergic disease is well established; however, the role of CD8(+) T cells (allergen-induced airway hyperresponsiveness (AHR) and inflammation) is less clear. This study was conducted to define the role of Ag-primed CD8(+) T cells in the development of these allergen-induced responses. CD8-deficient (CD8(-/-)) mice and wild-type mice were sensitized to OVA by i.p. injection and then challenged with OVA via the airways. Compared with wild-type. mice, CD8(-/-) mice developed significantly lower airway responsiveness to inhaled methacholine and lung eosinophilia, and exhibited decreased IL-13 production both in vivo, in the bronchoalveolar lavage (BAL) fluid, and in vitro, following Ag stimulation of peribronchial lymph node (PBLN) cells in culture. Reconstitution of sensitized and challenged CD8(-/-) mice with allergen-sensitized CD8(+) T cells fully restored the development of AHR, BAL cosinophilia, and IL-13 levels in BAL and in culture supernatants from PBLN cells. In contrast, transfer of naive CD8(+) T cells or allergen-sensitized CD8(+) T cells from IL-13-deficient donor mice failed to do so. Intracellular cytokine staining of lung as well as PBLN T cells revealed that CD8(+) T cells were a source of IL-13. These data suggest that Ag-primed CD8(+) T cells are required for the full development of AHR and airway inflammation, which appears to be associated with IL-13 production from these primed T cells. The Journal of Immunology, 2004, 172: 2549-2558.

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  • Respiratory syncytial virus-induced airway hyperresponsiveness is independent of IL-13 compared with that induced by allergen 査読

    JW Park, C Taube, ES Yang, A Joetham, A Balhorn, K Takeda, N Miyahara, A Dakhama, DD Donaldson, EW Gelfand

    JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY   112 ( 6 )   1078 - 1087   2003年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY, INC  

    Background: IL-13 is a central mediator of allergen-induced airway hyperresponsiveness, (AHR), but its role in respiratory syncytial virus (RSV)-induced AHR is not defined. The combination of allergen exposure and RSV infection is known to increase AHR and lung inflammation, but whether IL-13 regulates this increase is similarly not known.
    Objective: Our objective was to determine the role of RSV infection and IL-13 on airway responsiveness and lung inflammation on sensitized and challenged mice.
    Methods: Using a murine model of RSV infection and allergen exposure, we examined the role of IL-13 in the development of AHR and lung inflammation in IL-13 knockout mice, as well as using a potent IL-13 inhibitor (IL-13i). Mice were sensitized and challenged to allergen, and 6 days after the last challenge, they were infected with RSV. IL-13 was inhibited using an IL-13 receptor alpha(2)-human IgG fusion protein. AHR to inhaled methacholine was measured 6 days after infection, as was bronchoalveolar lavage fluid and lung inflammatory and cytokine responses.
    Results: RSV-induced AHR was unaffected by the IL-13i, despite prevention of goblet cell hyperplasia. Similar results were seen in IL-13-deficient mice. In sensitized and challenged mice, RSV infection significantly increased AHR, and after IL-13i treatment, AHR was significantly reduced, but to the levels seen in RSV-infected mice alone.
    Conclusions: These results indicate that despite some similarities, the mechanisms leading to AHR induced by RSV are different from those that follow allergen sensitization and challenge. Because IL-13 inhibition is effective in preventing the increases in AHR and mucus production in sensitized and challenged mice infected with RSV, IL-13i could play an important role in preventing the consequences of viral infection in patients with allergic asthma.

    DOI: 10.1016/j.jaci.2003.08.046

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  • Surfactant protein D regulates airway function and allergic inflammation through modulation of macrophage function 査読

    K Takeda, N Miyahara, YH Rha, C Taube, ES Yang, A Joetham, T Kodama, AM Balhorn, A Dakhama, C Duez, AJ Evans, DR Voelker, EW Gelfand

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   168 ( 7 )   783 - 789   2003年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER THORACIC SOC  

    The lung collectin surfactant protein D (SP-D) is an important component of the innate immune response but is also believed to play a role in other regulatory aspects of immune and inflammatory responses within the lung. The role of SP-D in the development of allergen-induced airway inflammation and hyperresponsiveness (AHR) is not well defined. SP-D levels progressively increased up to 48 hours after allergen challenge of sensitized mice and then subsequently decreased. The levels of SP-D paralleled the development of airway eosinophilia and AHR. To determine if this association was functionally relevant, mice were administered rat SP-D (rSP-D) intratracheally. When given to sensitized mice before challenge, AHR and eosinophilia were reduced by rSP-D in a dose-dependent manner but not by mutant rSP-D. rSP-D administration resulted in increased levels of interleukin (IL)-10, IL-12, and IFN-gamma in bronchoalveolar lavage fluid and reduced goblet cell hyperplasia. Culture of alveolar macrophages together with SP-D and allergen resulted in increased production of IL-10, IL-12, and IFN-gamma. These results indicate that SP-D can (negatively) regulate the development of AHR and airway inflammation after airway challenge of sensitized mice, at least in part, by modulating the function of alveolar macrophages.

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  • Pneumonitis induced by rifampicin 査読 国際誌

    N Kunichika, N Miyahara, K Kotani, H Takeyama, M Harada, M Tanimoto

    THORAX   57 ( 11 )   1000 - 1001   2002年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BRITISH MED JOURNAL PUBL GROUP  

    An 81 year old man was admitted to hospital with pulmonary Mycobocterium tuberculosis infection and was treated with rifampicin (UP), isoniazid (INH), and ethambutol (EB). On day 9 he developed fever and dyspnoea. Chest radiographs showed new infiltration shadows in the right lung. Bronchoalveolar lavage (BAL) was performed and increased numbers of lymphocytes were recovered. Drug induced pneumonitis was suspected so the antituberculous regimen was discontinued and methylprednisolone was administered. The symptoms and infiltration shadows improved. INH and EB were reintroduced without any recurrence of the abnormal shadows. T cell subsets in the BAL fluid and a positive lymphocyte stimulation test for RFP suggest that RFP induced pneumonitis may be related to a complex immunological response.

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  • Respiratory variation in superior vena cava flow in patients with chronic obstructive pulmonary disease: Estimation of pulmonary hypertension using Doppler flow index 査読 国際誌

    N Kunichika, N Miyahara, M Harada, M Tanimoto

    JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY   15 ( 10 )   1165 - 1169   2002年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MOSBY, INC  

    Patients with chronic obstructive pulmonary disease (COPD) are difficult to assess by conventional transthoracic echocardiography (TTE) because of emphysematous lungs or mediastinal deviation. We hypothesized that superior vena cava (SVC) flow is related to pulmonary circulation and may be useful for the detection of pulmonary hypertension (PH) in patients with COPD that cannot been assessed by direct evaluation using the tricuspid regurgitant Doppler velocity. SVC Doppler flow velocities were examined in 46 patients with COPD and the pressure gradient between the right ventricular and right atrial. pressure (RV-RADeltaP) was calculated by tricuspid regurgitant Doppler velocities. The patients were divided into 2 groups: 11 patients with PH (RV-RADeltaP &gt; 25 min Hg) were compared with 35 without PH. There was no significant difference in the maximal SVC peak systolic forward flow velocity during inspiration (INS) between these 2 groups. However, the minimal SVC peak systolic forward flow velocity during expiration (EXP) in the group with PH was significantly higher than that in the group without PH (37.4 +/- 20.0 cm/s vs 26.4 +/- 8.5 cm/s, P = .01). Linear regression analysis revealed a significant correlation between RV-RADeltaP and the EXP/INS ratio (r = 0.61, P &lt; .001). in COPD patients with PH, the increased expiratory SVC systolic flow supplemented the preload for the impaired right ventricular filling flow caused by PH, thereby maintaining the transtricuspid driving pressure. Our observation suggests that respiratory variation in SVC systolic forward flow may be a sensitive Doppler flow index for evaluating severity of PH in patients with COPD that cannot been assessed by conventional TTE.

    DOI: 10.1067/mje.2002.122355

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  • [Case of pulmonary Langerhans-cell histiocytosis]. 査読

    Sakugawa M, Tanimoto Y, Miyahara N, Kanehiro A, Kataoka M, Tanimoto M, Date H, Shimizu N, Yamadori I, Shibayama T

    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine   91 ( 9 )   2765 - 2767   2002年9月

  • [Orchiectomy for tuberculous epididymitis: a report of two cases with intractable to antituberculosis treatment].

    N Kunichika, K Murakami, K Makihata, K Takao, K Chikamori, K Aoe, N Miyahara, T Maeda, R Eda, H Takeyama

    Kekkaku : [Tuberculosis]   76 ( 10 )   673 - 6   2001年10月

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

    This paper describes two cases with tuberculous epididymitis. The first case was a 69-year-old man who was admitted to our hospital because of ulceration or right scrotum. Physical examination revealed a hard, rounded, a little bigger than egg-sized mass in the right scrotum. The second case was a 40-year-old man who was admitted to our hospital because of cough, fever and body weight loss. He was treated for pulmonary tuberculosis with isoniazid, rifampicin, streptomycin and pyrazinamide. Six months after admission, he complained of a painless swelling of the right scrotum. Physical examination revealed a hard, rounded, more than egg-sized mass in the right scrotum. Right orchiectomy was performed in these two cases, and they were cured.

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  • Pulmonary lymphoma of large B-cell type mimicking Wegener's granulomatosis 査読

    N Miyahara, R Eda, Y Umemori, T Murakami, N Kunichika, K Makihata, K Aoe, K Murakami, H Takeyama, M Harada

    INTERNAL MEDICINE   40 ( 8 )   786 - 790   2001年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPAN SOC INTERNAL MEDICINE  

    A 27-year-old man with a primary pulmonary lymphoma of large B-cell type is described. Symptoms involved both the upper and lower respiratory tract. A chest roentgenogram showed a dense mass with cavitation. Transbronchial biopsy specimens revealed no atypical cells, rather they demonstrated granulomatous infiltration and vasculitis consistent with but not conclusively diagnostic of Wegener's granulomatosis. The pulmonary mass became smaller after sulfamethoxazole-trimethoprim therapy. These features suggested Wegener's granulomatosis. However, an open biopsy specimen was diagnostic for diffuse lymphoma of large B-cell type. High-grade pulmonary lymphoma should be considered in the differential diagnosis of patients with clinical and pathologic features suggesting Wegener's granulomatosis.

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  • Compound heterozygosity for alpha-1-antitrypsin (S(iiyama) and QO(clayton)) in an Oriental patient.

    N Miyahara, K Seyama, T Sato, Y Fukuchi, R Eda, H Takeyama, M Harada

    Internal medicine (Tokyo, Japan)   40 ( 4 )   336 - 40   2001年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Alpha-1-antitrypsin (alpha1AT) deficiency is extremely rare among Orientals. We treated a 37-year-old man with severe pulmonary emphysema associated with a low serum concentration of alpha1AT. Mutation analysis of the alpha1AT gene was performed using a reverse transcription-polymerase chain reaction followed by sequencing. The patient proved to be a compound heterozygote carrying a S(iiyama) deficient allele and a QO(clayton) null allele. This is the first Japanese case of alpha1AT deficiency to arise from such compound heterozygosity in a family with no apparent consanguineous marriage, suggesting that the gene frequency for deficient alleles might be somewhat higher than previously estimated.

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  • Effects of short-term pulmonary rehabilitation on exercise capacity and quality of life in patients with chronic obstructive pulmonary disease.

    N Miyahara, R Eda, H Takeyama, N Kunichika, M Moriyama, K Aoe, H Kohara, K Chikamori, T Maeda, M Harada

    Acta medica Okayama   54 ( 4 )   179 - 84   2000年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Although the rehabilitation of patients with chronic obstructive pulmonary disease (COPD) improves both exercise capacity and quality of life, a standard protocol for COPD patients has not been established. To clarify whether physiologic and quality-of-life improvements can be achieved by an inpatient pulmonary rehabilitation program 5 days per week for 3 weeks, 18 patients with COPD were enrolled in a rehabilitation program. The physical exercise training regimen consisted of respiratory muscle stretch gymnastics and cycle ergometer exercise training. Pulmonary function tests, an incremental ergometer exercise test, a 6-min walking test, and a quality of life assessment by the Chronic Respiratory Questionnaire were administered before and after the program. The peak VO2, an indicator of maximal exercise capacity, did not increase, although the 6-min walking distance, an indicator of functional exercise capacity, increased significantly after rehabilitation. There was a significant improvement in the quality of life in terms of dyspnea, fatigue, and emotional state. These findings suggest that even a 3-week program may be beneficial for COPD patients. Increases in functional exercise capacity, even without an increase in maximal exercise capacity, are helpful for reducing dyspnea and improving quality of life parameters in patients with COPD.

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  • Cardiorespiratory responses during cycle ergometer exercise with different ramp slope increments in patients with chronic obstructive pulmonary disease.

    N Miyahara, R Eda, H Takeyama, T Maeda, K Aoe, N Kunichika, H Kohara, M Harada

    Internal medicine (Tokyo, Japan)   39 ( 1 )   15 - 9   2000年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    OBJECTIVE: The ramp exercise test has been widely used to evaluate cardiopulmonary responses to an incremental exercise load. This study was performed to clarify whether different slopes of the ramp exercise test influence exercise tolerance, exercise limiting factors, and respiratory pattern in patients with chronic obstructive pulmonary disease (COPD). SUBJECTS AND METHODS: We applied three different slopes (5 W/min, 10 W/min and 20 W/min) of the ramp exercise test in 9 patients with COPD and evaluated cardiopulmonary responses. RESULTS: There were no significant differences in peak oxygen uptake, anaerobic threshold (AT), minute ventilation, heart rate, arterial oxygen saturation, expired tidal volume, or respiratory rate at the maximal load among the three different ramp exercises tested. AT could be determined in six of nine patients (67%) at the slope of 5 W/min, in 8/9 (89%) at the slope of 10 W/min, and in 9/9 (100%) at the slope of 20 W/min. CONCLUSION: The findings suggest that the ramp slope does not affect exercise tolerance, exercise limiting factors, or respiratory patterns and each of these ramp slopes is useful for the evaluation of COPD. Ramp slopes of 10 W/ min or 20 W/min should be appropriate for the determination of AT.

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  • Bronchial atresia with transient spontaneous disappearance of a mucocele.

    N Miyahara, R Eda, S Makihara, T Maeda, K Aoe, N Kunichika, H Kohara, H Takeyama, M Harada

    Internal medicine (Tokyo, Japan)   38 ( 12 )   974 - 8   1999年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    We report the transient spontaneous disappearance of a mucocele due to bronchial atresia. Two years before presentation, a chest radiograph showed a hyperlucent right upper lung and a mucocele near the right hilum. A chest radiograph taken 1 year later showed that the mucocele had disappeared leaving an ovoid outline of a dilated bronchus. A chest radiograph obtained 3 months before presentation showed that the mucocele was present again. Atresia of the B3b bronchus of the right upper lobe was noted on thoracotomy. The "disappearance" of the mucocele probably was due to the clearance of mucoid material through collateral airways.

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書籍等出版物

  • 私の治療. 好酸球性肺炎

    妹尾聡, 宮原信明

    週間日本医事新報 p38-39  2022年1月 

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  • 新規生物学的製剤:抗IL-33抗体

    妹尾聡, 宮原信明

    呼吸器内科 科学評論社  2022年1月 

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  • 医学と医療の最前線 COPD、気管支喘息に対する吸入療法の進歩

    妹尾 賢, 宮原 信明( 担当: 共著)

    日本内科学会雑誌  2021年7月 

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  • アレルギー性気管支肺真菌症(ABPM)

    宮原信明( 担当: 単著)

    呼吸器疾患最新の治療 2021-22  2021年 

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  • 気管支拡張症

    宮原 信明( 担当: 単著)

    今日の治療指針  2021年 

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  • 閉塞性細気管支炎

    妹尾賢, 宮原信明( 担当: 共著)

    見る診るわかる!胸部画像診断  2021年 

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  • 新型コロナウイルス感染症

    谷口暁彦, 宮原信明

    見る診るわかる!胸部画像診断  2021年 

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  • 【重症喘息治療の現在-生物学的製剤を活用した症状コントロール-】GINAにおける生物学的製剤の位置づけ

    宮原信明( 担当: 単著)

    Progress in Medicine  2020年4月 

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  • 【アレルギーと脂質メディエーター アップデート】LTB4とアレルギー

    宮原 信明( 担当: 共著)

    アレルギー・免疫 25(3) 362-370  2018年2月 

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  • 【傷害関連分子パターンとアレルギー疾患】Receptor for advanced glycation end-products(RAGE)と喘息

    宮原 信明( 担当: 共著)

    臨床免疫・アレルギー科 66(2) 141-145 2016年8月  2016年8月 

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MISC

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講演・口頭発表等

  • 当院においてメプリズマブを使用した重症気管支喘息症例の検討

    岩本佳隆, 谷口暁彦, 小田尚廣, 板野純子, 妹尾賢, 金廣有彦, 木浦勝行, 前田嘉信, 宮原信明

    第1回日本アレルギー学会中国四国地方会 

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    開催年月日: 2019年2月2日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:広島  

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  • EGFR exon18,delE709 T710insD変異陽性肺腺癌に対してafatinibが奏功した1例

    山岡 主知、岩本 佳隆、市原 英基、二宮 貴一朗、谷口 暁彦、頼 冠名、大橋 圭明、宮原 信明、久保 寿夫、田端 雅弘、堀田 勝幸、木浦 勝行、前田 嘉信

    第60回日本呼吸器学会中国・四国地方会  2018年 

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    開催年月日: 2018年12月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:高松市  

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  • Important Contribution of Neuropeptide Y to House Dust Mite-Induced Airway Hyperresponsiveness and Inflammation

    Akihiko Taniguchi, Naohiro Oda, Daisuke Morichika, Satoru Senoo, Utako Fujii, Misako Shibakura, Yoshinobu Maeda, Katsuyuki Kiura, Arihiko Kanehiro, Nobuaki Miyahara

    XXIV World Congress of Asthma  2018年 

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    開催年月日: 2018年10月3日 - 2018年10月6日

    記述言語:英語   会議種別:ポスター発表  

    開催地:東京  

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  • 抗IL-5抗体を使用したアレルギー性気管支肺アスペルギルス症・好酸球性副鼻腔炎合併重症喘息の一例

    谷口 暁彦, 妹尾 賢, 小田 尚廣, 板野 純子, 久保 寿夫, 宮原 信明, 前田 嘉信, 金廣 有彦, 木浦 勝行

    第30回中国・四国臨床アレルギー研究会  2018年 

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    開催年月日: 2018年8月26日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:岡山  

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  • 体外式膜型人工肺(ECMO)導入により救命し得た加熱式タバコによる重症急性好酸球性肺炎の1例

    安東 愛理、谷口 暁彦、中須賀 崇匡、安東 千裕、原 尚史、梅野 貴裕、岩本 佳隆、二宮 貴一朗、久保 寿夫、市原 英基、大橋 圭明、堀田 勝幸、宮原 信明、田端 雅弘、青景 聡之、塚原 紘平、内藤 宏道、中尾 篤典、前田 嘉信、木浦 勝行

    第59回日本呼吸器学会中国・四国地方会  2018年 

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    開催年月日: 2018年7月14日 - 2018年7月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:出雲市  

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  • 肺動脈塞栓血栓症を合併した全身状態不良の肺腺癌に対しpembrolizumabが奏効した1例

    濱崎 友洋,中須賀 崇匡,大橋 圭明,安東 千裕,原 尚史,梅野 貴裕,岩本 佳隆,板野 純子,二宮 貴一朗,二宮 崇,谷口 暁彦,久保 寿夫,市原 英基,堀田 勝幸,宮原 信明,田端 雅弘,前田 嘉信,木浦 勝行

    第59回日本呼吸器学会中国・四国地方会  2018年 

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    開催年月日: 2018年7月14日 - 2018年7月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:島根  

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  • ニボルマブ投与による尋常性乾癬・ぶどう膜炎の顕在化

    河野 和馬 , 妹尾 賢, 大橋 圭明, 中須賀 崇匡, 安東 千裕, 原 尚史, 岩本 佳隆, 梅野 貴裕, 二宮 貴一朗, 谷口 暁彦, 二宮 崇, 久保 寿夫, 市原 英基, 頼 冠名, 片山 英樹, 堀田 勝幸, 宮原 信明, 田端 雅弘, 前田 嘉信, 木浦 勝行

    第59回日本呼吸器学会中国・四国地方会,第57回日本肺癌学会中国・四国支部学術集会  2018年 

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    開催年月日: 2018年7月14日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:出雲  

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  • フェンタニルとミダゾラム併用による気管挿管下での気管支鏡検査の苦痛度評価

    南 大輔、瀧川 奈義夫、二宮 崇、久保 寿夫、市原 英基、大橋 圭明、堀田 勝幸、宮原 信明、柴山 卓夫、田端 雅弘、木浦 勝行

    第41回日本呼吸器内視鏡学会学術集会  2018年 

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    開催年月日: 2018年5月24日 - 2018年5月25日

    記述言語:日本語  

    開催地:東京  

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  • 多発結節影を呈した特発性器質化肺炎の1例

    飯尾享平 , 板野純子, 大橋圭明, 肥後寿夫,谷口暁彦, 宮原信明, 木浦勝行, 前田嘉信

    第118回 日本内科学会中国支部主催 中国地方会  2018年 

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    開催年月日: 2018年5月19日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:鳥取  

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  • 多発結節影を呈した特発性器質化肺炎の1例

    飯尾 亨平、板野 純子、谷口 暁彦、大橋 圭明、肥後 寿夫、宮原 信明、木浦 勝行、前田 嘉信

    第118回 日本内科学会中国支部主催 中国地方会  2018年 

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    開催年月日: 2018年5月19日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:米子  

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  • Contribution of IL33 for Protective Effects Against Elastase-Induced and Cigarette Smoke Extract-Induced Emphysema

    Daisuke Morichika, Nobuaki Miyahara, Akihiko Taniguchi, Naohiro Oda, Utako Fujii, Satoru Senoo, Mikio Kataoka, Toshiaki Okada, Masayuki Hanaoka, Tomohiro Yoshimoto, Mitsune Tanimoto, Yoshinobu Maeda, Katsuyuki Kiura, Arihiko Kanehiro

    American Thoracic Society International Conference 2018  2018年 

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    開催年月日: 2018年5月18日 - 2018年5月23日

    記述言語:英語   会議種別:ポスター発表  

    開催地:San Diego, CA, USA  

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  • Neuropeptide Y Is Required for the Development of Type-2 Responses and Allergen-Induced Airway Hyperresponsiveness and Inflammation

    Naohiro Oda, Nobuaki Miyahara, Akihiko Taniguchi, Daisuke Morichika, Satoru Senoo, Utako Fujii, Misako Shibakura, Yoshinobu Maeda, Katsuyuki Kiura, Arihiko Kanehiro

    American Thoracic Society International Conference 2018  2018年 

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    開催年月日: 2018年5月18日 - 2018年5月23日

    記述言語:英語   会議種別:ポスター発表  

    開催地:San Diego, CA, USA  

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  • Protective effects of IL-33 against elastase-induced and cigarette smoke extract-induced emphysema

    Akihiko Taniguchi, Daisuke Morichika, Nobuaki Miyahara, Utako Fujii, Naohiro Oda, Satoru Senoo, Mikio Kataoka, Toshiaki Okada, Masayuki Hanaoka, Tomohiro Yoshimoto, Mitsune Tanimoto, Yoshinobu Maeda, Katsuyuki Kiura, Arihiko Kanehiro

    第58回日本呼吸器学会学術講演会  2018年 

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    開催年月日: 2018年4月27日 - 2018年4月29日

    記述言語:英語   会議種別:ポスター発表  

    開催地:大阪  

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  • Contribution of neuropeptide Y to house dust mite-induced airway hyperresponsiveness and inflammation

    Naohiro Oda, Nobuaki Miyahara, Daisuke Morichika, Akihiko Taniguchi, Satoru Senoo, Utako Fujii, Mikio Kataoka, Mitsune Tanimoto, Yoshinobu Maeda, Katsuyuki Kiura, Arihiko Kanehiro

    第58回日本呼吸器学会学術講演会  2018年 

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    開催年月日: 2018年4月27日 - 2018年4月29日

    記述言語:英語   会議種別:ポスター発表  

    開催地:大阪  

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  • 異なる臨床病型を呈した Osimertinib による薬剤性肺障害の検討

    鬼塚拡平 , 板野純子, 大橋圭明, 市原英基, 堀田勝幸, 宮原信明, 田端雅弘, 谷本 安 , 金廣有彦, 木浦勝行

    第58回日本呼吸器学会中国・四国地方会  2017年 

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    開催年月日: 2017年10月28日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:広島  

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  • メポリズマブが著効したアレルギー性 気管支肺アスペルギルス症の一例

    藤本周作, 妹尾賢, 小田尚廣, 谷口暁彦, 板野純子, 久保寿夫, 宮原信明, 前田嘉信, 金廣有彦, 木浦勝行

    第58回日本呼吸器学会中国四国地方会  2017年 

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    開催年月日: 2017年10月28日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:広島  

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  • 異なる臨床病型を呈した Osimertinib による薬剤性肺障害の検討

    (鬼塚 拡平)、板野 純子、大橋 圭明、市原 英基、堀田 勝幸、宮原 信明、田端 雅弘、谷本 安、金廣 有彦、木浦 勝行

    第58回日本呼吸器学会中国・四国地方会  2017年 

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    開催年月日: 2017年10月28日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:広島  

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  • EBUS-TBNA後の発熱および穿刺針洗浄培養における挿管チューブの有用性

    南 大輔、瀧川 奈義夫、 沖 昌英、坂 英雄 、二宮 崇、久保 寿夫、市原 英基、大橋 圭明、佐藤 晃子、堀田 勝幸、宮原 信明、柴山 卓夫、田端 雅弘、木浦 勝行

    第58回日本肺癌学会学術集会  2017年 

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    開催年月日: 2017年10月14日 - 2017年10月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:横浜  

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  • 器質化肺炎パターンを呈した第3世代EGFRチロシンキナーゼ阻害薬による薬剤性肺障害の1例

    板野純子, 大橋圭明, 中西将元, 谷口暁彦, 宮原信明, 金廣有彦, 木浦勝行

    第29回中国・四国臨床アレルギー研究会  2017年 

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    開催年月日: 2017年9月3日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:岡山  

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  • 器質化肺炎と類似した肺陰影を呈し,鑑別を要した肺動脈血管肉腫の一例

    安原大貴 , 渡邉洋美, 久保寿夫, 田端雅弘, 大橋圭明, 堀田勝幸, 宮原信明, 金廣有彦, 木浦勝行

    第57回日本呼吸器学会中国・四国地方会  2017年 

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    開催年月日: 2017年7月14日 - 2017年7月15日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:高知  

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  • 抗炎症性メディエーターと炎症・アレルギー

    宮原信明

    第66回日本アレルギー学会学術大会  2017年 

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    開催年月日: 2017年6月17日

    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:東京  

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  • アレルギー性気道炎症におけるNeuropeptide Yの役割

    小田尚廣, 宮原信明, 森近大介, 藤井詩子, 谷口暁彦, 金廣有彦

    第66回日本アレルギー学会学術大会  2017年 

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    開催年月日: 2017年6月16日 - 2017年6月18日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • 抗炎症性メディエーターと炎症・アレルギー

    宮原 信明

    第66回日本アレルギー学会学術大会  2017年 

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    開催年月日: 2017年6月

    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:東京  

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  • Safety and Discomfort During Bronchoscopy Performed Under Sedation with Fentanyl and Midazolam: A Prospective Study

    Daisuke Minami?,?Nagio Takigawa?,?Takashi Ninomiya?,?Toshio Kubo?,?Eiki Ichihara?,?Kadoaki Ohashi?,?Akiko Sato?,?Katsuyuki Hotta?,?Takuo Shibayama?,?Nobuaki Miyahara?,?Masahiro Tabata?,?Arihiko Kanehiro?,?Katsuyuki Kiura

    American Thoracic Society International Conference 2017  2017年 

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    開催年月日: 2017年5月19日 - 2017年5月24日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Washington DC, USA  

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  • Clinical Characteristics of Japanese Candidates for Lung Transplant Due to Interstitial Lung Disease and Risk Factors for Early Death While on the Waiting List

    H. Higo, E. Ichihara, T. Kurosaki, K. Miyoshi, T. Kubo, S. Otani, S. Sugimoto, M. Yamane, N. Miyahara, K. Kiura, T. Oto

    American Thoracic Society International Conference 2017  2017年 

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    開催年月日: 2017年5月19日 - 2017年5月24日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Washington DC, USA  

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  • Effect of a Retinoid X Receptor Partial Agonist on the Development of Emphysema and Airway Inflammation in a Murine Model of Emphysema

    Daisuke Morichika?,?Arihiko Kanehiro?,?Hiroki Kakuta?,?Akihiko Taniguchi?,?Utako Fujii?,?Naohiro?Oda?,?Nobuaki Miyahara,?Katsuyuki Kiura?,?Mitsune Tanimoto

    American Thoracic Society International Conference 2017  2017年 

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    開催年月日: 2017年5月19日 - 2017年5月24日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Washington DC, USA  

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  • 進行膵癌に対するゲムシタビン+ナブパクリタキセル併用療法における薬剤性肺障害の検討

    久保寿夫, 狩野裕久, 妹尾 賢, 西井和也, 秦 雄介, 渡邉洋美, 二宮 崇, 市原英基, 大橋圭明, 佐藤晃子, 加藤博也 , 堀田勝幸, 宮原信明, 田端雅弘, 金廣有彦, 木浦勝行

    第57回日本呼吸器学会学術講演会  2017年 

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    開催年月日: 2017年4月21日 - 2017年4月23日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • 間質性肺疾患による脳死肺移植登録患者の臨床像と待機期間中早期死亡リスク因子の検討

    肥後寿夫, 市原英基, 黒崎毅史 , 久保寿夫, 大橋圭明, 勝田知也, 洲脇俊充, 宮原信明, 三好新一郎, 大藤剛宏 , 木浦勝行

    第57回日本呼吸器学会学術講演会  2017年 

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    開催年月日: 2017年4月21日 - 2017年4月23日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • 器質化肺炎と類似した肺陰影を呈し診断まで時間を要した肺動脈血管肉腫の一例

    松尾聡子 , 渡邉洋美, 久保寿夫, 田端雅弘, 妹尾賢, 大橋圭明, 西森久和, 堀田勝幸, 宮原信明 木浦勝行

    第114回日本内科学会総会  2017年 

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    開催年月日: 2017年4月14日 - 2017年4月16日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • 気管支喘息,COPDの基礎と臨床:さまざまなEffector cellの関与 招待

    宮原信明

    呼吸の今と未来を考える講演会  2017年 

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    開催年月日: 2017年4月11日

    記述言語:日本語   会議種別:口頭発表(招待・特別)  

    開催地:松本市  

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  • 進行膵癌に対するゲムシタビン+ナブパクリタキセル併用療法における薬剤性肺障害の検討

    久保 寿夫, 狩野 裕久, 妹尾 賢, 西井 和也, 秦 雄介, 渡邉 洋美, 二宮 崇, 市原 英基, 大橋 圭明, 佐藤 晃子, 加藤 博也 , 堀田 勝幸, 宮原 信明, 田端 雅弘, 金廣 有彦, 木浦 勝行

    第57回日本呼吸器学会学術講演会  2017年 

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    開催年月日: 2017年4月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • 間質性肺疾患による脳死肺移植登録患者の臨床像と待機期間中早期死亡リスク因子の検討

    肥後寿夫,市原英基, 黒崎毅史 ,久保寿夫,大橋圭明, 勝田知也 , 洲脇俊充 ,宮原信明, 三好新一郎 , 大藤剛宏 ,木浦勝行

    第57回日本呼吸器学会学術講演会  2016年 

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    開催年月日: 2017年4月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • 抗酸菌感染症との鑑別を要した膵神経内分泌腫瘍肺転移の1例

    松尾 聡子 , 狩野 裕久, 佐藤 晃子, 妹尾 賢, 西井 和也, 秦 雄介, 渡邉 洋美, 二宮 崇, 久保 寿夫, 市原 英基, 大橋 圭明, 堀田 勝幸, 宮原 信明, 田端 雅弘, 金廣 有彦, 谷本 光音, 木浦 勝行

    第57回日本呼吸器学会中国四国地方会  2016年 

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    開催年月日: 2016年12月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:岡山  

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  • pulmonary tumor thrombotic microangiopathy(PTTM)が疑われた乳癌によるびまん性微小腫瘍塞栓の1例?

    安東 愛理 , 谷口 暁彦, 二宮 崇, 市原 英基, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行, 溝尾 妙子

    第56回日本呼吸器学会中国四国地方会  2016年 

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    開催年月日: 2016年12月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:岡山  

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  • T790M陽性非小細胞肺癌の癌性髄膜炎に対してエルロチニブが著効した一例?

    山田 光太郎 , 市原 英基, 妹尾 賢, 渡邉 洋美, 狩野 裕久, 西井 和也, 秦 雄介, 二宮 崇, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 金廣 有彦, 木浦 勝行, 堀田 勝幸, 宮原 信明, 谷本 光音

    第56回日本呼吸器学会中国四国地方会  2016年 

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    開催年月日: 2016年12月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:岡山  

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  • Recent topics of molecular biology in the field of airway inflammation 招待

    Miyahara N

    21th Congress of Asian Pacific Society of Respirology 2016  2016年 

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    開催年月日: 2016年11月13日

    記述言語:英語   会議種別:口頭発表(招待・特別)  

    開催地:Thailand  

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  • IL-23 is Essential to the Development of Elastase-induced Pulmonary Inflammation and Emphysema

    Fujii U, Kanehiro A, Kakuta H, Taniguchi A, Oda N, Morichika M, Ikeda G, Koga H, Waseda K, Kurimoto E, Miyahara N, Kataoka M, Tanimoto M

    European Respiratory Society International Conference 2016  2016年 

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    開催年月日: 2016年9月

    記述言語:英語   会議種別:ポスター発表  

    開催地:England  

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  • オシメルチニブ投与中に発症したうっ血性心不全の一例

    松尾 逸平 , 渡邉 洋美, 市原 英基, 狩野 裕久, 妹尾 賢, 西井 和也, 秦 雄介, 二宮 崇, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行

    第55回日本肺癌学会中国四国支部会  2016年 

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    開催年月日: 2016年7月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:広島  

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  • 進行膵癌に対するゲムシタビン+ナブパクリタキセル併用療法における薬剤性肺障害の検討?

    古谷 奈緒 , 久保 寿夫, 田端 雅弘, 秦 雄介, 狩野 裕久, 渡邉 洋美, 妹尾 賢, 西井 和也, 二宮 崇, 市原 英基, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 木浦 勝行, 片山 英樹, 谷本 光音

    第55回日本呼吸器学会中国四国地方会  2016年 

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    開催年月日: 2016年7月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:広島  

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  • 肺多形癌に対してnivolumabを投与中にニューモシスチス肺炎を発症した1例

    (小柳太作), 妹尾 賢, 狩野 裕久, 西井 和也, 秦 雄介, 渡邉 洋美, 二宮 崇, 久保 寿夫, 大橋 圭明, 市原 英基, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行

    第55回日本呼吸器学会中国・四国地方会  2016年 

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    開催年月日: 2016年7月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:広島  

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  • 器質化肺炎様の画像所見を呈した過敏性肺臓炎の1例

    (安藤 明美),早稲田 公一,灘 隆宏,木村耕介,頼 冠名,(岩室雅也,花山宜久),宮原信明

    第115回日本内科学会中国地方会  2016年 

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    開催年月日: 2016年6月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:岡山  

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  • The Role of Retinoid X Receptor in allergen-induced Airway Inflammation in Mice

    Fujii U, Kanehiro A, Kakuta H, Taniguchi A, Oda N, Morichika M, Ikeda G, Koga H, Waseda K, Kurimoto E, Miyahara N, Kataoka M, Tanimoto M

    第65回日本アレルギー学会学術大会  2016年 

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    開催年月日: 2016年6月

    記述言語:英語   会議種別:ポスター発表  

    開催地:東京  

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  • フェンタニルとミダゾラム併用による気管支鏡検査の苦痛度評価

    南 大輔, 二宮 崇, 久保 寿夫, 大橋 圭明, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行, 瀧川 奈義夫

    第39回日本呼吸器内視鏡学会学術集会  2016年 

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    開催年月日: 2016年6月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:名古屋  

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  • RebiopsyにおいてEBUS-TBNAが有用であった3症例?

    狩野 裕久, 南 大輔, 妹尾 賢, 西井 和也, 秦 雄介, 渡邉 洋美, 加藤 有加, 谷口 暁彦, 二宮 崇, 久保 寿夫, 大橋 圭明, 堀田 勝幸, 宮原 信明, 田端 雅弘, 金廣 有彦, 谷本 光音, 木浦 勝行

    第39回日本呼吸器内視鏡学会学術集会  2016年 

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    開催年月日: 2016年6月

    記述言語:日本語   会議種別:ポスター発表  

    開催地:名古屋  

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  • 肺クリプトコッカス症診断における迅速細胞診を用いた気管支鏡検査の有性

    森近 大介, 南 大輔, 宮原 信明, 谷口 暁彦, 二宮 崇, 久保 寿夫, 大橋 圭明, 堀田 勝幸, 田端 雅弘, 金廣 有彦, 谷本 光音, 木浦 勝行

    第39回日本呼吸器内視鏡学会学術集会  2016年 

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    開催年月日: 2016年6月

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:名古屋  

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  • Treatment With Novel Retinoid X Receptor Partial Agonist Attenuates Eosinophilic Airway Inflammation And Airway Hyperresponsiveness

    Fujii U, Kanehiro A, Kakuta H, Taniguchi A, Oda N, Morichika M, Ikeda G, Koga H, Waseda K, Kurimoto E, Miyahara N, Kataoka M, Tanimoto M

    American Thoracic Society International Conference 2016  2016年 

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    開催年月日: 2016年5月

    記述言語:英語   会議種別:ポスター発表  

    開催地:San Francisco  

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  • 成人気管支喘息における好酸球性中耳炎合併の実態についての検討

    谷本 安, 板野 純子, 石賀 充典, 難波 史代, 田中 寿明, 小野 勝一郎, 高橋 秀治, 濱田 昇, 河田 典子, 木村 五郎, 宗田 良, 宮原 信明, 木浦 勝行, 谷本 光音

    第56回日本呼吸器学会学術講演会  2016年 

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    開催年月日: 2016年4月11日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:京都  

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  • IL-23 is Essential to the Development of Elastase-induced Pulmonary Inflammation and Emphysema

    Fujii U, Miyahara N, Taniguchi A, Waseda K, Morichika D, Kurimoto E, Koga H, Kataoka M, Gelfand EW , Cua DJ , Yoshimura A, Tanimoto M, Kanehiro A

    第56回日本呼吸器学会学術講演会  2016年 

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    開催年月日: 2016年4月11日

    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:京都  

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  • アレルギー性気道炎症マウスモデルにおけるレチノイドX受容体(RXR)パーシャルアゴニストの治療効果に関する研究

    藤井 詩子, 金廣 有彦, 谷口 暁彦, 森近 大介, 小田 尚廣, 栗本 悦子, 古賀 光, 早稲田 公一, 加来田 博貴 , 宮原 信明, 木浦 勝行, 谷本 光音

    第56回日本呼吸器学会学術講演会  2016年 

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    開催年月日: 2016年4月11日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:京都  

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  • Inter-Assembly Symposium of Allergy, Immunology and Inflammation between ATS and JRS. Requirement for the receptor for advanced glycation end-products (RAGE) in allergic airway inflammation and COPD.

    Nobuaki Miyahara

    第56回日本呼吸器学会学術講演会  2016年 

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    開催年月日: 2016年4月

    記述言語:英語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:京都  

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  • 気管支喘息の病態と最新の治療

    宮原 信明

    獣医アトピー・アレルギー・免疫学会シンポジウム  2017年 

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    開催年月日: 2016年1月10日

    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:東京  

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  • ボリュームアナライザーSYNAPSE VINCENTを用いたガイドシース併用気管支腔内 超音波断層法の肺癌診断への導入効果

    南 大輔、瀧川奈義夫、槇本 剛、狩野裕久、秦 雄介、渡邊洋美、 中西将元、二宮 崇、久保寿夫、大橋圭明、堀田勝幸、宮原信明、 金廣有彦、田端雅弘、谷本光音、木浦勝行

    第54回日本呼吸器学会中国・四国地方会,第24回日本呼吸器内視鏡学会中国四国支部会,第66回日本結核病学会中国四国支部会  2015年 

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    開催年月日: 2015年12月19日 - 2015年12月20日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:島根  

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  • 全身状態不良のALK融合遺伝子陽性肺癌患者に対しアレクチニブが奏効した2例

    為房宏輔、秦 雄介、狩野裕久、渡邉洋美、槇本 剛、中西将元、加藤有加、 南 大輔、二宮 崇、谷口暁彦、久保寿夫、大橋圭明、堀田勝幸、宮原信明、 田端雅弘、金廣有彦、谷本光音、木浦勝行

    第54回日本呼吸器学会中国・四国地方会,第24回日本呼吸器内視鏡学会中国四国支部会,第66回日本結核病学会中国四国支部会  2015年 

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    開催年月日: 2015年12月19日 - 2015年12月20日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:島根  

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  • 化学放射線療法後に外科的切除を行い、長期生存が得られた肺癌症例に発症した慢性進 行性肺アスペルギルス症の2例

    吉川真生、狩野裕久、秦 雄介、渡邉洋美、中西将元、槇本 剛、 加藤有加、南 大輔、谷口暁彦、二宮 崇、久保寿夫、大橋圭明、 堀田勝幸、宮原信明、金廣有彦、田端雅弘、谷本光音、木浦勝行

    第54回日本呼吸器学会中国・四国地方会,第24回日本呼吸器内視鏡学会中国四国支部会,第66回日本結核病学会中国四国支部会  2015年 

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    開催年月日: 2015年12月19日 - 2015年12月20日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:島根  

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  • Effect of retinoid X receptor partial agonist on airway inflammation and hyperresponsiveness

    Utako Fujii, Arihiko Kanehiro, Daisuke Morichika, Akihiko Taniguchi, Etsuko Murakami, Kouichi Waseda, Hikari Nakayama, Hiroki Kakuta, Nobuaki Miyahara, Mitsune Tanimoto

    欧州呼吸器学会国際会議  2015年 

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    開催年月日: 2015年9月26日 - 2015年9月30日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Amsterdam  

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  • Receptor for advanced glycation end-products on structural cells controls allergic airway inflammation

    宮原 信明, 谷口 暁彦, 早稲田 公一,栗本 悦子, 藤井詩子, 谷本 安、片岡 幹男, 山本靖彦、山本 博, 谷本 光音, 金廣 有彦

    第25回国際喘息学会日本・北アジア部会  2015年 

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    開催年月日: 2015年9月3日 - 2015年9月4日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:横浜  

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  • 肺類上皮血管内皮腫の一例

    田中晶平,小田尚廣,佐藤晃子,宮原信明,狩野裕久, 中西将元,秦雄介,槇本剛,久保寿夫,大橋圭明,堀田勝幸,田端雅弘,金廣有彦,谷本光音,木浦勝行

    第53回日本呼吸器学会中国・四国地方会,第54回日本肺癌学会中国・四国支部会  2015年 

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    開催年月日: 2015年7月3日 - 2015年7月4日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:愛媛  

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  • ぶどう膜炎を契機に発症し、診断に至った完全型Heerfordt症候群の1例

    吉川真生、槇本 剛、宮原信明、小田尚廣、狩野裕久、中西将元、 秦 雄介、久保寿夫、大橋圭明、二宮 崇、堀田勝幸、金廣有彦、 田端雅弘、谷本光音、木浦勝行

    第53回日本呼吸器学会中国・四国地方会,第54回日本肺癌学会中国・四国支部会  2015年 

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    開催年月日: 2015年7月3日 - 2015年7月4日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:愛媛  

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  • 薬疹、薬剤性肺炎を治療経過で認めた胸腺癌にnab-paclitaxel単剤療法が有用であった1例

    河合三津保、南 大輔、槇本 剛、中西将元、小田尚廣、豊田容輔、 肥後寿夫、二宮 崇、久保寿夫、大橋圭明、佐藤晃子、堀田勝幸、 宮原信明、金廣有彦、田端雅弘、谷本光音、木浦勝行

    第53回日本呼吸器学会中国・四国地方会,第54回日本肺癌学会中国・四国支部会  2015年 

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    開催年月日: 2015年7月3日 - 2015年7月4日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:愛媛  

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  • BIOEVALUATOR?を用いた迅速細胞診断を併用した超音波気管支鏡ガイド下針生検の有用性

    南大輔, 瀧川 奈義夫, 槇本 剛, 小田 尚廣, 豊田 容輔, 二宮 貴一朗, 肥後 寿夫, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行

    第38回日本呼吸器内視鏡学会学術集会  2015年 

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    開催年月日: 2015年6月11日 - 2015年6月12日

    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:東京  

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  • PET-CTにて縦隔、肺門リンパ節転移偽陽性の肺癌症例における超音波気管支鏡ガイド下針生検の有用性

    南大輔, 瀧川 奈義夫, 小田 尚廣, 槇本 剛, 二宮 貴一朗, 豊田 容輔, 肥後 寿夫, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行

    第38回日本呼吸器内視鏡学会学術集会  2015年 

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    開催年月日: 2015年6月11日 - 2015年6月12日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • ガイドシース併用気管支腔内超音波断層法による経気管支肺生検で確定診断された肺悪性リンパ腫の2例

    肥後寿夫, 南 大輔, 小田 尚廣, 豊田 容輔, 二宮 貴一朗, 槇本 剛, 谷口 暁彦, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 田端 雅弘, 金廣 有彦, 谷本 光音, 木浦 勝行

    第38回日本呼吸器内視鏡学会学術集会  2015年 

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    開催年月日: 2015年6月11日 - 2015年6月12日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • 腎移植後の免疫抑制療法に合併した肺クリプトコッカス症の診断にEBUS-GSが有用であった1例

    槇本 剛, 南 大輔, 宮原 信明, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行

    第38回日本呼吸器内視鏡学会学術集会  2015年 

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    開催年月日: 2015年6月11日 - 2015年6月12日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • 経気管支肺生検にて悪性リンパ腫と確定診断された4例

    小田 尚廣, 南 大輔, 瀧川 奈義夫, 槙本 剛, 二宮 貴一郎, 豊田 容輔, 肥後 寿夫, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行

    第38回日本呼吸器内視鏡学会学術集会  2015年 

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    開催年月日: 2015年6月11日 - 2015年6月12日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • エラスターゼ誘導マウスCOPDモデルにおける抗IL-23抗体の抑制効果の検討

    藤井詩子, 宮原 信明, 谷口 暁彦, 川野 香, 森近 大介, 栗本 悦子, 早稲田 公一, 古賀 光, 片岡 幹男, 木浦 勝行, 谷本 光音, 吉村 昭彦, 金廣 有彦

    第64回日本アレルギー学会学術集会  2015年 

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    開催年月日: 2015年5月26日 - 2015年5月28日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • Importance of IL-23 to the Development of Elastase-Induced Pulmonary Inflammation and Emphysema

    Utako Fujii, Nobuaki Miyahara, Akihiko Taniguchi, Kaoru Kawano, Daisuke Morichika, Etsuko Murakami, Kouichi Waseda, Hikari Nakamura, Mikiko Kataoka, Akihiko Yoshimura, Mitsune Tanimoto, Arihiko Kanehiro

    米国胸部学会国際会議  2015年 

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    開催年月日: 2015年5月15日 - 2015年5月21日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Denver  

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  • A Retrospective Analysis of the Background of Patients with Pulmonary Cryptococcosis and Diagnostic Methods Used

    Daisuke Morichika, Nobuaki Miyahara

    米国胸部学会国際会議  2015年 

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    開催年月日: 2015年5月15日 - 2015年5月21日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Denver  

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  • BIOEVALUATOR(R)を用いた迅速細胞診断を併用したEBUS-TBNAの有用性

    槇本剛, 南 大輔, 瀧川 奈義夫, 二宮 貴一朗, 小田 尚廣, 豊田 容輔, 肥後 寿夫, 久保 寿夫, 大橋 圭明, 佐藤 晃子, 堀田 勝幸, 宮原 信明, 金廣 有彦, 田端 雅弘, 谷本 光音, 木浦 勝行

    第55回日本呼吸器学会学術講演会  2015年 

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    開催年月日: 2015年4月17日 - 2015年4月19日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • エラスターゼ誘導気道炎症及び肺気腫進展における抗IL-23抗体の抑制効果の検討

    藤井 詩子, 宮原 信明, 川野 香, 谷口 暁彦, 森近 大介, 栗本 悦子, 早稲田 公一, 古賀 光, 片岡 幹男, 木浦 勝行, 谷本 光音, 吉村 昭彦, 金廣 有彦

    第55回日本呼吸器学会学術講演会  2015年 

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    開催年月日: 2015年4月17日 - 2015年4月19日

    記述言語:日本語   会議種別:ポスター発表  

    開催地:東京  

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  • 経気管支肺生検にて悪性リンパ腫と確定診断された4例

    小田尚廣, 宮原信明, 木浦勝行

    第24回日本呼吸器内視鏡学会中国四国支部会  2015年 

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    開催年月日: 2015年2月28日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:高知  

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  • ガイドシース併用気管支腔内超音波断層法で診断した関節リウマチに伴う肺アミロイドーシスの1例

    白石雄太郎,小田尚廣,槇本 剛,二宮貴一朗,豊田容輔,南 大輔,宮原信明,金廣有彦,谷本光音,木浦勝行

    第52回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年12月13日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 遺伝性出血性末梢血管拡張症による肺動静脈瘻にMycobacterium avium complex症を合併した1例

    羽田野 裕,南 大輔,二宮貴一朗,小田尚廣,豊田容輔,槇本 剛,肥後寿夫,大橋圭明,佐藤晃子,藤原廣康,堀田勝幸,宮原信明,金廣有彦,田端雅弘,金澤 右,谷本光音,木浦勝行

    第52回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年12月13日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • CT上明らかな異常陰影を呈さず経気管支肺生検で診断し得た肺Intravascular Lymphomatosisの2例

    山本 晃,二宮貴一朗,谷口暁彦,南 大輔,久保寿夫,大橋圭明,佐藤晃子,堀田勝幸,宮原信明,金廣有彦,谷本光音,木浦勝行

    第52回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年12月13日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • ガイドシース併用気管支腔内超音波断層法の肺癌診断への導入効果

    南 大輔,瀧川奈義夫,二宮貴一朗,小田尚廣,豊田容輔,槇本 剛,肥後寿夫,久保寿夫,大橋圭明,佐藤晃子,堀田勝幸,宮原信明,金廣有彦,田端雅弘,谷本光音,木浦勝行

    第55回日本肺癌学会学術集会 

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    開催年月日: 2014年11月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 肺梗塞による血痰で発症した抗リン脂質抗体症候群の1例

    上堀昌代,豊田容輔,宮原信明,藤原英晃,久保寿夫,西森久和,近藤英生,金廣有彦,谷本光音,木浦勝行

    日本内科学会中国支部主催 第111回中国地方 

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    開催年月日: 2014年11月8日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • ACTH産生胸腺神経内分泌腫瘍に合併したニューモシスチス肺炎の1例

    枝木久典,南 大輔,二宮貴一朗,小田尚廣,豊田容輔,槇本 剛,肥後寿夫,小松原基志,久保寿夫,大橋圭明,佐藤晃子,稲垣謙一,堀田勝幸,宮原信明,金廣有彦,田端雅弘,谷本光音,木浦勝行

    第51回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年7月12日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • マウスアレルギー性気道炎症モデルにおける終末糖化産物受容体(RAGE)の役割

    谷口 暁彦,宮原 信明,金廣 有彦,早稲田 公一,栗本 悦子,藤井詩子,谷本 安,片岡幹男,木浦 勝行,(山本 靖彦,山本 博),谷本 光音

    第51回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年7月12日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 岡山大学における新入生のアレルギー疾患の調査

    古賀光,(岩?良章),金廣有彦,宮原信明,(河原宏子),(清水幸登),(大西勝),谷本光音,(小倉俊郎)

    第26回日本アレルギー学会春季臨床大会 

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    開催年月日: 2014年7月12日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • マウスアレルギー性気道炎症モデルにおける終末糖化産物受容体(RAGE)の役割

    谷口暁彦,宮原信明,金廣有彦,早稲田公一,村上悦子,藤井詩子,谷本 安,片岡幹男,木浦勝行,山本靖彦,山本 博,谷本光音

    第51回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年7月12日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 間質性肺炎が先行し,筋炎所見を欠く抗PL-7抗体陽性抗ARS抗体症候群の1例

    神原由依,二宮貴一朗,宮原信明,豊田容輔,谷口暁彦,南 大輔,久保寿夫,大橋圭明,佐藤晃子,堀田勝幸,金廣有彦,山村裕理子,谷本光音,木浦勝行

    第51回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年7月12日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 桂枝茯苓丸による薬剤性肺炎の1例

    福見拓也,二宮貴一朗,大橋圭明,谷口暁彦,南 大輔,久保寿夫,佐藤晃子,堀田勝幸,宮原信明,金廣有彦,谷本光音,木浦勝行

    第51回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年7月12日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 子宮頚癌に合併した急速に進行する間質性肺炎と心嚢液貯留を伴った多発性筋炎の一例

    上堀晶代,田村朋季,宮原信明,谷口暁彦,南 大輔,久保寿夫,大橋圭明,佐藤晃子,堀田勝幸,田端雅弘,金廣有彦,谷本光音,木浦勝行

    第51回日本呼吸器学会中国・四国地方会 

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    開催年月日: 2014年7月12日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Requirement for the receptor for advanced glycation end-products on airway structural cells in allergen-induced airway inflammation

    A.Taniguchi, N.Miyahara, A.Kanehiro, K.Waseda, E.Kurimoto, U.Fujii, Y.Tanimoto, M.Kataoka, (Y. Yamamoto, E.W. Gelfand , H. Yamamoto), M.Tanimoto

    2014米国呼吸器学会 

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    開催年月日: 2014年5月18日

    記述言語:英語   会議種別:口頭発表(一般)  

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  • 肺気腫と肺気腫合併喘息マウスに対するロイコトリエン受容体拮抗薬の効果.

    池田元洋, 金廣有彦, 宮原信明, 古賀 光, 淵本康子, 早稲田公一, 栗本悦子, 谷口暁彦, 片岡幹男, 谷本光音.

    第54回日本呼吸器学会学術講演会 

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    開催年月日: 2014年4月25日 - 2014年4月27日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 皮疹を伴う不明熱として発症し間質性肺炎発症をきっかけに診断に至った抗Jo-1抗体陰性皮膚筋炎の一例.

    (松田文子), 田村朋季, 二宮貴一朗, 後藤田裕子, 森近大介, 萱谷紘枝, 宮原信明, 金廣有彦, 木浦勝行, 谷本 安, 谷本光音

    第54回日本呼吸器学会学術講演会 

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    開催年月日: 2014年4月25日 - 2014年4月27日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 肺腺癌に合併し診断に苦慮した急性肺クリプトコッカス症の1例.

    (森田 絢子), 二宮貴一朗, 南 大輔, 堀田勝幸, 宮原信明, 谷本光音, 木浦勝行, (入江真大, 葉山牧夫, 山本寛斎, 三好新一郎)

    第54回日本呼吸器学会学術講演会 

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    開催年月日: 2014年4月25日 - 2014年4月27日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 肺癌に酷似する画像所見を呈したtafro症候群の1例.

    (水田萌子), 二宮貴一朗, 市原英基, 堀田勝幸, 谷本 安, 宮原信明, 田端雅弘, 南 大輔, 金廣有彦, 木浦勝行, 松岡賢市, 谷本光音, (岩城憲子)

    第54回日本呼吸器学会学術講演会 

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    開催年月日: 2014年4月25日 - 2014年4月27日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Clinical studies of patients with pulmonary cryptococcosis in this hospital mainly with respect to their back grounds and diagnostic methods.

    Daisuke Morichika, Daisuke Minami, Akihiro Taniguchi, Toshio Kubo, Katsuyuki Hotta, Nobuaki Miyahara, Arihiko Kanehiro, Mitsune Tanimoto, Katsuyuki Kiura

    American Thoracic Society 

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    開催年月日: 2014年4月25日

    記述言語:英語   会議種別:口頭発表(一般)  

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  • PP496 当院で経験した肺クリプトコッカス症の患者背景と診断法の検討

    森近大介, 南大輔, 谷口暁彦, 久保寿夫, 堀田勝幸, 宮原信明, 金廣有彦, 谷本光音, 木浦勝行

    第54回日本呼吸器学会学術講演会 

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    開催年月日: 2014年4月25日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 超音波気管支鏡ガイド下針生検(EBUS-TBNA)におけるBIOEVALUATORRを使用した迅速細胞診断の効果

    二宮貴一朗,南 大輔,瀧川奈義夫,森近大介,後藤田裕子,萱谷紘枝,田村朋季,久保寿夫,佐藤晃子,堀田勝幸,宮原信明,金廣有彦,田端雅弘,谷本光音,木浦勝行

    第37回日本呼吸器内視鏡学会 

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    開催年月日: 2014年4月14日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 肺癌診断におけるガイドシース併用気管支腔内超音波断層法の導入効果

    南 大輔,瀧川奈義夫,二宮貴一朗,森近大介,後藤田裕子,萱谷紘枝,田村朋季,久保寿夫,佐藤晃子,堀田勝幸,宮原信明,金廣有彦,田端雅弘,谷本光音,木浦勝行

    第37回日本呼吸器内視鏡学会 

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    開催年月日: 2014年4月14日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 肺腺癌に合併し診断に苦慮した続発性クリプトコッカス症の2例

    森近 大介, 南 大輔, 二宮貴一郎, 堀田勝幸, 宮原信明, 田端雅弘, 谷本光音, 木浦勝行, (入江 真大, 葉山 牧夫, 山本 寛斎, 三好 新一郎)

    第22回気管支内視鏡学会中国四国支部会 

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    開催年月日: 2014年2月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 肺腺癌に合併し診断に苦慮した続発性クリプトコッカス症の2例.

    森近 大介, 南 大輔, 二宮貴一郎, 堀田勝幸, 宮原信明, 田端雅弘, 谷本光音, 木浦勝行, (入江 真大, 葉山 牧夫, 山本 寛斎, 三好 新一郎)

    第22回日本呼吸器内視鏡学会中国四国支部会 

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    開催年月日: 2014年2月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Effect of neutrophil elastase inhibitor on airway inflammation and airway hyperresponsiveness in a murine model of asthma

    Koga H, Kanehiro A, Miyahara N, Fuchimoto Y, Ikeda G, Waseda K, Tanimoto Y, Kataoka M, Tanimoto M

    ERS Annual Congress 

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    開催年月日: 2009年9月12日 - 2009年9月16日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Vienna  

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  • EThe role of CCR5 in allergen-induced airway hyperresponsiveness and airway inflammation

    Fuchimoto Y, Kanehiro A, Miyahara N, Koga H, Ikeda G, Waseda K, (Matsushima K, Gelfand EW), Tanimoto M

    ERS Annual Congress 

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    開催年月日: 2009年9月12日 - 2009年9月16日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Vienna  

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  • The PBMC of severe asthmantics showed enhanced candida antigen induced IL-5, IL-13 and TARC production and this enhancement was inhibited by dendric cells deprition

    Okada C, Hirano A, Tanimoto Y, Kimura G, Miyahara N, Kanehiro A, Soda R, Takahashi K

    ERS Annual Congress 

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    開催年月日: 2009年9月12日 - 2009年9月16日

    記述言語:英語   会議種別:ポスター発表  

    開催地:Vienna  

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  • The role of leukotriene B4 in both mast-cell independent and dependent allergic airway responses

    Miyahara N, (Ohnishi H, Miyahara S), Takeda K, Waseda K, Kurimoto E, Ikeda G, Fuchimoto Y, Nojima D, Tanimoto Y, Kanehiro A, Kataoka M, Tanimoto M, (Gelfand EW)

    第19回国際喘息学会日本北アジア部会 

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    開催年月日: 2009年7月10日

    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • COPDおよびCOPD合併喘息に対するロイコトリエン受容体拮抗薬の効果について

    池田元洋, 金廣有彦, 宮原信明, 早稲田公一, 古賀 光, 渊本康子, 近藤稔人, 小野勝一郎, 平野 淳, 谷本 安, 片岡幹男, 谷本光音

    第19回国際喘息学会日本北アジア部会 

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    開催年月日: 2009年7月10日

    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • Secondary allergen challenge mouse modelにおける好中球エラスターゼ阻害薬の効果

    古賀 光, 金廣有彦, 宮原信明, 早稲田公一, 池田元洋, 渊本康子, 小野勝一郎, 平野 淳, 谷本 安, 片岡幹男, 谷本光音

    第19回国際喘息学会日本北アジア部会 

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    開催年月日: 2009年7月10日

    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • 乳癌に対する放射線照射後に発症したBOOP症候群の臨床的検討

    谷本 安, 久山彰一, 高尾和志, 岸 俊行, 堀田勝幸, 瀧川奈義夫, 宮原信明, 金廣有彦, 田端雅弘, 木浦勝行, 片岡幹男, 谷本光音

    第49回日本呼吸器学会学術講演会 

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    開催年月日: 2009年6月14日 - 2009年6月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • Requirement for leukotriene B4 in both mast-cell independent and dependent allergic airway responses

    Miyahara N, (Miyahara S, Ohnishi H), Takeda K, Waseda K, Ikeda G, Koga H, Fuchimoto Y, Tanimoto Y, Kanehiro A, Kataoka M, Tanimoto M, (Gelfand EW)

    第49回日本呼吸器学会学術講演会 

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    開催年月日: 2009年6月14日 - 2009年6月15日

    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • ロイコトリエン受容体拮抗薬のCOPDおよび喘息合併COPDモデルに対する効果の検討

    池田元洋, 金廣有彦, 宮原信明, 早稲田公一, 古賀 光, 渊本康子, 小野勝一郎, 平野 淳, 谷本 安, 片岡幹男, 谷本光音

    第49回日本呼吸器学会学術講演会 

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    開催年月日: 2009年6月14日 - 2009年6月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • 慢性閉塞性肺疾患(COPD)を合併した進行肺非小細胞癌(NSCLC)の予後

    原田大二郎, 瀧川奈義夫, 木浦勝行, 谷本 安, 堀田勝幸, 平木章夫, 宮原信明, 田端雅弘, 金廣有彦, 谷本光音

    第49回日本呼吸器学会学術講演会 

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    開催年月日: 2009年6月14日 - 2009年6月15日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:東京  

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  • 自己汗により誘発された慢性蕁麻疹の1例

    能島大輔, 谷本 安, 栗本悦子, 本多宣裕, 宮原信明, 金廣有彦, 木浦勝行, 谷本光音, 片岡幹男

    第100回日本内科学会中国地方会 

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    開催年月日: 2009年5月30日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:第17回日本呼吸器内視鏡学会中国四国支部会 2009.2.22(高松)  

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  • 非乾酪性類上皮細胞肉芽腫病変を伴ったために診断に苦慮したホジキンリンパ腫の1例

    栗本悦子, 谷本 安, 瀧川奈義夫, 二宮 崇, 能島大輔, 村上斗司, 本多宣裕, 堀田勝幸, 宮原信明, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音, 片岡幹男

    第32回日本呼吸器内視鏡学会学術集会 

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    開催年月日: 2009年5月28日 - 2009年5月30日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:第17回日本呼吸器内視鏡学会中国四国支部会 2009.2.22(高松)  

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  • 血液悪性腫瘍の治療中に出現した胸部異常影に対する気管支鏡検査

    村上斗司, 瀧川奈義夫, 谷本 安, 二宮 崇, 栗本悦子, 能島大輔, 本多宣裕, 堀田勝幸, 宮原信明, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音

    第32回日本呼吸器内視鏡学会学術集会 

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    開催年月日: 2009年5月28日 - 2009年5月30日

    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:第17回日本呼吸器内視鏡学会中国四国支部会 2009.2.22(高松)  

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  • Adoptive Transfer of Leukotriene A4 Hydrolase (LTA4H)-Sufficient Mast Cells Restores the Development of IgE-Mediated Airway Hyperresponsiveness in LTA4H-Deficient Mice

    (H. Ohnishi), N. Miyahara, (J.E. Loader, A. Joetham, Dakhama), Takeda, (E.W. Gelfand)

    105th 2009 Annual meeting of American Thoracic Society 

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    開催年月日: 2009年5月20日

    会議種別:ポスター発表  

    開催地:San Diego, California, USA  

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  • Role of the Leukotriene B4 Pathway in Established Asthma,

    K. Waseda, N. Miyahara, A. Kanehiro, G. Ikeda, Y. Fuchimoto, H. Koga, Y. Tanimoto, M. Kataoka, K. Takeda, M. Tanimoto, (E.W. Gelfand)

    105th 2009 Annual meeting of American Thoracic Society, San Diego, California, USA 

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    開催年月日: 2009年5月19日

    会議種別:ポスター発表  

    開催地:San Diego, California, USA  

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  • Effect of Cysteinyl Leukotriene Receptor Antagonist for Murine Models of COPD and Bronchial Asthma Associated with COPD

    G. Ikeda, A. Kanehiro, N. Miyahara, H. Koga, Y. Fuchimoto, K. Waseda, K. Ono, A. Hirano, Y. Tanimoto, M. Kataoka, M. Tanimoto

    105th 2009 Annual meeting of American Thoracic Society 

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    開催年月日: 2009年5月19日

    会議種別:ポスター発表  

    開催地:San Diego, California, USA  

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  • 気管支鏡検査で診断されたリッキシマブ併用化学療法中のニューモシスチス肺炎

    栗本悦子, 能島大輔, 新谷勝美, 瀧川奈義夫, 村上斗司, 二宮 崇, 本多宣裕, 堀田勝幸, 宮原信明, 谷本 安, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音

    第17回日本呼吸器内視鏡学会中国四国支部会 2009.2.22(高松) 

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    開催年月日: 2009年4月

    会議種別:口頭発表(一般)  

    開催地:第17回日本呼吸器内視鏡学会中国四国支部会 2009.2.22(高松)  

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  • 気管支鏡下生検で診断された19年後の再発乳癌の1例

    村上斗司, 木浦勝行, 瀧川奈義夫, 能島大輔, 本多宣裕, 二宮 崇, 栗本悦子, 堀田勝幸, 宮原信明, 谷本 安, 田端雅弘, 金廣有彦, 谷本光音

    第17回日本呼吸器内視鏡学会中国四国支部会 2009.2.22(高松) 

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    開催年月日: 2009年4月

    会議種別:口頭発表(一般)  

    開催地:第17回日本呼吸器内視鏡学会中国四国支部会 2009.2.22(高松)  

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  • 肺サルコイドーシス治療におけるメソトレキサート(MTX)の有用性に関する検討

    谷本 安, 中田安成, 片岡幹男, 早稲田公一, 池田元洋, 渊本康子, 古賀 光, 市川裕久, 宮原信明, 金廣有彦, 森 由弘, 谷本光音

    第58回日本アレルギー学会秋季学術大会 2008.11.29(東京) 

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    開催年月日: 2008年11月29日

    会議種別:口頭発表(一般)  

    開催地:東京  

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  • アレルギー性気道炎症におけるCCR5の役割について

    渊本康子, 金廣有彦, 宮原信明, 古賀 光, 池田元洋, 早稲田公一, 谷本 安, 片岡幹男, 谷本光音, (松島綱治)

    第58回日本アレルギー学会秋季学術大会 2008.11.28(東京) 

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    開催年月日: 2008年11月28日

    会議種別:口頭発表(一般)  

    開催地:東京  

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  • Confirmation of the Essential Role of LTB4 in Airway Hyperresponnsiveness Using LTA4H-Dificient Mice

    Miyahara N, (Miyahara S, Ohnishi H), Takeda K, Waseda K, Ikeda G, Fuchimoto Y, Koga H, Tanimoto Y, Kanehiro A, Kataoka M, Tanimoto M, (Gelfand E)

    第58回日本アレルギー学会秋季学術大会 2008.11.27(東京) 

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    開催年月日: 2008年11月27日

    会議種別:口頭発表(一般)  

    開催地:東京  

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  • 呼吸器科医と非呼吸器科医の間の喫煙率と患者に対する禁煙指導の差異に関する検討

    藤原義朗, 徳田佳之, 木浦勝行, 瀧川奈義夫, 堀田勝幸, 宮原信明, 谷本 安, 金廣有彦,田端雅弘, 谷本光音

    第43回日本呼吸器学会中国四国地方会 2008.7.19(高知) 

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    開催年月日: 2008年7月19日

    会議種別:口頭発表(一般)  

    開催地:高知  

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  • ロイコトリエンB4受容体(BLT1)および樹状細胞のアレルギー性気道反応における役割の検討

    宮原信明, (大西広志, 松田弘之, 宮原聡子), 武田勝行, 早稲田公一, 池田元洋, 渊本康子, 古賀 光, 谷本 安, 金廣有彦, 片岡幹男, 谷本光音, (Gelfand EW)

    第43回日本呼吸器学会中国四国地方会 2008.7.18(高知) 

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    開催年月日: 2008年7月18日

    会議種別:口頭発表(一般)  

    開催地:高知  

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  • アレルギー性気管支肺アスペルギルス症(ABPA)の治療経過中に播種性アスペルギルス症を発症した1例

    原田大二郎, 瀧川奈義夫, (大崎幸七, 沖本二郎, 肥後貴子, 寺戸通久, 佐藤康晴), 本多宣裕, 堀田勝幸, 宮原信明, 谷本 安, 金廣有彦, 田端雅弘, 木浦勝行, 谷本光音

    第43回日本呼吸器学会中国四国地方会 2008.7.18(高知) 

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    開催年月日: 2008年7月18日

    会議種別:口頭発表(一般)  

    開催地:高知  

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  • 大柴胡湯による薬剤誘起性肺炎

    八杉昌幸, 宮原信明, 尾瀬 功, 越智宣昭, 原田大二郎, 本多宣裕, 堀田勝幸, 瀧川奈義夫, 田端雅弘, 谷本 安, 金廣有彦, 木浦勝行, 片岡幹男, 谷本光音

    第43回日本呼吸器学会中国四国地方会 2008.7.18(高知) 

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    開催年月日: 2008年7月18日

    会議種別:口頭発表(一般)  

    開催地:高知  

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  • Requirememt for the leukotriene B4 receptor-1(BLT1) on dendritic cells in the development of allergen-induced airway hyperresponsiveness and inflammation

    Miyahara N, (Matsuda H, Ohnishi H, Miyahara S), Takeda K, Waseda K, Fuchimato Y, Koga H, Ikeda G, Tanimoto Y, Kanehiro A, Kataoka M,

    第48回日本呼吸器学会学術講演会 2008.6.15(神戸) 

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    開催年月日: 2008年6月15日

    会議種別:口頭発表(一般)  

    開催地:神戸  

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  • 高齢者サルコイドーシスの臨床

    市川裕久, 宮原信明, 谷本 安, 金廣有彦, 森 由弘, 片岡幹男, 中田安成, 谷本光音

    第48回日本呼吸器学会学術講演会 2008.6.15(神戸) 

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    開催年月日: 2008年6月15日

    会議種別:口頭発表(一般)  

    開催地:神戸  

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  • 肺サルコイドーシスにおけるMethotrexate(MTX)治療の検討-プレドニゾロン(PDS)減量による再燃例への併用効果-

    谷本 安, 中田安成, 片岡幹男, 早稲田公一, 池田元洋, 渊本康子, 古賀 光, 市川裕久, 宮原信明, 金廣有彦, 森 由弘, 谷本光音

    第48回日本呼吸器学会学術講演会 2008.6.15(神戸) 

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    開催年月日: 2008年6月15日

    会議種別:口頭発表(一般)  

    開催地:神戸  

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  • ゲフィチニブ単剤療法が施行された肺非小細胞癌における予後因子としての血清KL-6

    藤原義朗, 木浦勝行, 瀧川奈義夫, (豊岡伸一), 堀田勝幸, (宗 淳一), 宮原信明, 谷本 安, 金廣有彦, 田端雅弘, (加藤勝也, 伊達洋至), 谷本光音

    第48回日本呼吸器学会学術講演会 2008.6.15(神戸) 

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    開催年月日: 2008年6月15日

    会議種別:口頭発表(一般)  

    開催地:神戸  

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  • The role of CCR5 in allergen-induced airway inflammation and airway hy-perresponsiveness

    Futimoto Y, Kanehiro A, Miyahara N, Koga H, Ikeda G, Waseda K, (Matsushima K, Gelfand EW), Tanimoto M

    第48回日本呼吸器学会学術講演会 2008.6.15(神戸) 

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    開催年月日: 2008年6月15日

    会議種別:口頭発表(一般)  

    開催地:神戸  

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  • 喘息患者指導における医師,薬剤師の連携に関する調査研究

    岡田千春, 平野 淳, 木村五郎, 谷本 安, 金廣有彦, 宮原信明, 宗田 良, 高橋 清

    第20回日本アレルギー学会春季臨床大会 2008.6.13(東京) 

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    開催年月日: 2008年6月13日

    会議種別:口頭発表(一般)  

    開催地:東京  

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  • 高齢者喘息の管理における喘息コントロールテスト(ACT)の有用性に関する検討

    谷本 安, 渊本康子, 尾形佳子, 早稲田公一, 金澤 聰, 宮原信明, 金廣有彦, 片岡幹男, 高橋 清, 谷本光音

    第20回日本アレルギー学会春季臨床大会 2008.6.12(東京) 

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    開催年月日: 2008年6月12日

    会議種別:口頭発表(一般)  

    開催地:東京  

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  • モンテカルストが有効であった高齢者好酸救性胃腸炎の1例

    平野 淳, 岡田千春, 木村五郎, 谷本 安, 金廣有彦, 宮原信明, 片岡幹男, 宗田 良, 高橋 清

    第20回日本アレルギー学会春季臨床大会 

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    開催年月日: 2008年6月12日

    会議種別:口頭発表(一般)  

    開催地:東京  

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  • ペグインターフェロン(PEG-IFN)が原因と考えられた薬剤性肺障害の1例

    越智宣昭, 谷本 安, 宮原信明, 瀧川奈義夫, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音, 玉置明彦, (山本和秀)

    第98回日本内科学会中国地方会 2008.5.31(山口) 

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    開催年月日: 2008年5月31日

    会議種別:口頭発表(一般)  

    開催地:山口  

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  • 骨融解を生じた播種性真菌症

    (肥後貴子, 寺戸通久), 原田大二郎, 瀧川奈義夫, 宮原信明, 谷本 安, 金廣有彦, 木浦勝行, 谷本光音, (佐藤康晴)

    第98回日本内科学会中国地方会 2008.5.31(山口) 

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    開催年月日: 2008年5月31日

    会議種別:口頭発表(一般)  

    開催地:山口  

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  • Neutrophil Elastase Inhibitor Attenuates Allergen-Induced Airway Inflammation and Airway Hyperresponsiveness in a Model of Secondary Allergen Challenge

    H. Koga, M.D., A. Kanehiro, M.D., Ph, N. Miyahara, M.D., Ph, G. Ikeda, M.D., Y. Fuchimoto, M.D., K. Waseda, M.D., K. Ono, M.D., A. Hirano, M.D., Ph, E.W. Gelfand, M.D., M. Tanimoto, M.D., Ph

    ATS meeting (Annual meeting of American Thoracic Society) 2008 

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    開催年月日: 2008年5月21日

    会議種別:ポスター発表  

    開催地:Toronto、 Canada  

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  • Requirement for CCR5 Expression on T Cells in Allergen-Induced Airway Inflammation

    Y. Fuchimoto, M.D., A. Kanehiro, M.D., Ph, N. Miyahara, M.D., Ph, H. Koga, M.D., G. Ikeda, M.D., K. Waseda, M.D., K. Matsushima, M.D., Ph, E.W. Gelfand,

    ATS meeting (Annual meeting of American Thoracic Society) 2008 

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    開催年月日: 2008年5月19日

    会議種別:ポスター発表  

    開催地:Toronto、 Canada  

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  • Differential Effects of SP-D and SP-A in the Development of Ozone-Induced Airway Hyperresponsiveness

    K. Takeda, M.D., Ph.D., S. Matsubara, Ph.D., H. Matsuda, M.D., Ph, N. Miyahara, M.D., Ph, G. McConville, M.S., A. Joetham, B.S., A. Dakhama, Ph.D., R.J. Mason, M.D., E.W. Gelfand, M.D.,

    ATS meeting (Annual meeting of American Thoracic Society) 2008 

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    開催年月日: 2008年5月19日

    会議種別:ポスター発表  

    開催地:Toronto、 Canada  

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  • Conversion of Naturally Occurring CD4+CD25+ Regulatory T Cell Function Following Ligation of Glucocorticoid-Induced TNF Receptor (GITR)

    A.A. Joetham, B.S., S. Matsubara, Ph.D., M. Okamoto, M.D., Ph, K. Takeda, M.D., Ph, N. Miyahara, M.D., Ph, A. Dakhama, Ph.D., E.W. Gelfand, M.D

    ATS meeting (Annual meeting of American Thoracic Society) 2008 

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    開催年月日: 2008年5月18日

    会議種別:ポスター発表  

    開催地:Toronto、 Canada  

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  • Requirement for Leukotriene B4 Release from Mast Cells in the Development of IgE-Mediated Airway Hyperresponsiveness

    N. Miyahara, S. Miyahara, K. Takeda,S. Matsubara, H. Onishi, H. Matsuda, M. Okamoto,J. Loader,A. Joetham,A. Dakhama, E.W. Gelfand,

    ATS meeting (Annual meeting of American Thoracic Society) 2008 

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    開催年月日: 2008年5月18日

    会議種別:ポスター発表  

    開催地:Toronto、 Canada  

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  • Extracellular Signal-Regulated Kinase 1/2-Dependent Pathways Are Essential for Effector Memory CD8+ T Cell-Mediated Airway Hyperresponsiveness and Inflammation

    H. Ohnishi, M.D., Ph.D., K. Takeda, M.D., Ph, J.J. Lucas, Ph.D., J. Domenico, B.A., N. Miyahara, M.D., Ph, M. Okamoto, M.D., Ph, A. Dakhama, Ph.D., E.W. Gelfand, M.D

    ATS meeting (Annual meeting of American Thoracic Society) 2008 

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    開催年月日: 2008年5月18日

    会議種別:ポスター発表  

    開催地:Toronto、 Canada  

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  • 大腸癌術後、消化管MALTリンパ腫の経過観察中に胸部異常陰影および頚部リンパ節腫脹を認めた一例

    柏原宏美, 瀧川奈義夫, 池田和眞, 谷本 安, 堀田勝幸, 宮原信明, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音

    第72回岡山胸部疾患懇話会 2008.9.16(岡山) 

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    開催年月日: 2008年4月

    会議種別:口頭発表(一般)  

    開催地:第72回岡山胸部疾患懇話会 2008.9.16(岡山)  

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  • ニューモシスチス肺炎加療中にST合剤による薬剤性肺炎を合併したと考えられた1例

    二宮 崇, 宮原信明, 遠西大輔, 堀田勝幸, 瀧川奈義夫, 田端雅弘, 谷本 安, 金廣有彦, 木浦勝行, 谷本光音

    第99回日本内科学会中国地方会 2008.11.8(米子) 

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    開催年月日: 2008年4月

    会議種別:口頭発表(一般)  

    開催地:第99回日本内科学会中国地方会 2008.11.8(米子)  

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  • 慢性閉塞性肺疾患(COPD)を合併した進行肺非小細胞癌(NSCLC)の予後

    原田大二郎, 瀧川奈義夫, 木浦勝行, 谷本 安, 堀田勝幸, 平木章夫, 宮原信明, 田端雅弘, 金廣有彦, 谷本光音

    第99回日本内科学会中国地方会 2008.11.8(米子) 

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    開催年月日: 2008年4月

    会議種別:口頭発表(一般)  

    開催地:第99回日本内科学会中国地方会 2008.11.8(米子)  

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  • 高齢者サルコイドーシスと若年者サルコイドーシスの比較検討

    市川裕久, 中田安成, 宮原信明, 谷本 安, 金廣有彦, 森 由弘, 片岡幹男, 谷本光音

    第28回日本サルコイドーシス/肉腫性疾患学会総会 2008.11.8(仙台) 

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    開催年月日: 2008年4月

    会議種別:口頭発表(一般)  

    開催地:2008.11.8(仙台)  

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  • COPD及びCOPD合併喘息モデルに対するロイコトリエン受容体拮抗薬の効果について

    池田元洋, 金廣有彦, 宮原信明, 早稲田公一, 古賀 光, 渊本康子, 近藤稔人, 小野勝一郎, 平野 淳, 谷本 安, 片岡幹男, 谷本光音

    第58回日本アレルギー学会秋季学術大会 2008.11.27(東京) 

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    開催年月日: 2008年4月

    会議種別:口頭発表(一般)  

    開催地:第58回日本アレルギー学会秋季学術大会 2008.11.27(東京)  

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  • ペグインターフェロンa(PEG-IFN a)が原因と考えられた薬剤性肺障害の一例

    谷本 安, 越智宣昭, 玉置明彦, 早稲田公一, 渊本康子, 池田元洋, 古賀 光, 宮原信明, 金廣有彦, 片岡幹男, 谷本光音

    第20回中国・四国臨床アレルギー研究会 2008.8.30(岡山) 

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    開催年月日: 2008年4月

    会議種別:口頭発表(一般)  

    開催地:第20回中国・四国臨床アレルギー研究会 2008.8.30(岡山)  

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  • 背臥位から腹臥位へ撮影体位を変更することで陰影の移動を認めた肺胞蛋白症の1例

    市原英基, 瀧川奈義夫, 宮原信明, 谷本 安, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音, (加藤勝也, 山鳥一郎)

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年11月17日

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • 肺癌加療中に副腎転移より出血を来した2例

    武田洋正, 田端雅弘, 瀧川奈義夫, 宮原信明, 谷本 安, 金廣有彦, 木浦勝行, 谷本光音

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年11月17日

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • 藤原義朗, 木浦勝行, 瀧川奈義夫, 堀田勝幸, 宮原信明, 谷本 安, 金廣有彦, 田端雅弘, 谷本光音

    藤原義朗, 木浦勝行, 瀧川奈義夫, 堀田勝幸, 宮原信明, 谷本 安, 金廣有彦, 田端雅弘, 谷本光音

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年11月17日

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • 脳転移を契機に発見された肺原発絨毛癌の1例

    久保寿夫, 田端雅弘, 瀧川奈義夫, 宮原信明, 谷本 安, 金廣有彦, 木浦勝行, 谷本光音

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年11月17日

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • Garcin症候群を契機に発見された肺癌の一例

    藤井昌学, 木浦勝行, 瀧川奈義夫, 堀田勝幸, 宮原信明, 谷本 安, 金廣有彦, 田端雅弘, 谷本光音, (瀬原吉秀)

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年11月17日

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • 大柴胡湯によると思われる薬剤性肺障害の1例

    八杉昌幸, 宮原信明, 田端雅弘, 瀧川奈義夫, 谷本 安, 金廣有彦, 木浦勝行, 谷本光音

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年11月17日

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • マウスsecondary challenge喘息モデルに対する好中球エラスターゼ阻害薬の効果について

    古賀 光, 金廣有彦, 宮原信明, 早稲田公一, 池田元洋, 渊本康子, 近藤稔人, 小野勝一郎, 平野 淳, 谷本 安, 片岡幹男, 谷本光音

    第57回日本アレルギー学会秋季学術大会 2007.11.2(神奈川) 

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    開催年月日: 2007年11月2日

    会議種別:口頭発表(一般)  

    開催地:横浜  

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  • Antigen-DNA vaccine modulates airway reactivity and inflammation by antigen-specific CD8T expansion

    武田勝行, (Dow SW), 宮原信明, (小屋俊行, 児玉 拓, Dakhama A, Kedl RM, Gelfand EW)

    第57回日本アレルギー学会秋季学術大会 2007.11.1(神奈川) 

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    開催年月日: 2007年11月1日

    会議種別:口頭発表(一般)  

    開催地:横浜  

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  • アレルギー性鼻炎における即時型、遅延型反応での抗原特異性、非特異性の検討

    宮原聡子, *宮原信明, Gelfand EW

    第57回日本アレルギー学会秋季学術大会 2007.11.1(神奈川) 

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    開催年月日: 2007年11月1日

    会議種別:口頭発表(一般)  

    開催地:横浜  

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  • 気管支喘息におけるCD8T 細胞の役割

    宮原信明

    第10回癌と免疫セミナー 

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    開催年月日: 2007年9月20日

    開催地:岡山  

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  • ロイコトリエンの機能と制御

    宮原信明

    第6回 Asthma Forum in Okayama 

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    開催年月日: 2007年9月7日

    会議種別:口頭発表(一般)  

    開催地:岡山市  

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  • 気管支喘息におけるCD8T細胞の役割

    宮原信明

    岡山呼吸器疾患研究会 

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    開催年月日: 2007年8月25日

    開催地:岡山市  

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  • 乳癌に対する放射線照射後に発症したBOOPの臨床的検討

    谷本安、早稲田公一、淵本康子、金澤聡、尾形佳子、井上由佳里、佐久川亮、宮原信明、金廣有彦、片岡幹男、谷本光音

    第19回中国・四国臨床アレルギー研究会 

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    開催年月日: 2007年8月25日

    会議種別:口頭発表(一般)  

    開催地:岡山市  

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  • ロイコトリエンB4受容体およびのCD8T細胞の気道過敏性における役割の検討

    宮原信明、金廣有彦、谷本安、池田元洋、淵本康子、古賀光、瀧川奈義夫、田端雅弘、木浦勝行、Erwin Gelfand, 谷本光音

    日本呼吸器学会中国四国地方会 

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    開催年月日: 2007年7月6日

    開催地:広島市  

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  • 気道炎症、気道過敏性および気道リモデリングに対するPirfenidoneの抑制効果の検討

    平野 淳, 金廣有彦, 小野勝一郎, *宮原信明, 谷本 安, 片岡幹男, 谷本光音, 木村五郎, 岡田千春, 高橋 清

    第42回日本呼吸器学会中国四国地方会 2007.7.6(広島) 

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    開催年月日: 2007年7月6日

    会議種別:口頭発表(一般)  

    開催地:広島  

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  • ステロイド治療中にChurge-Strauss 症候群の2例

    早稲田公一、谷本安、岡田千春、柏原宏美、久保寿夫、武田洋正、藤井昌学、宮原信明、瀧川奈義夫、金廣有彦、田端雅弘、木浦勝行、谷本光音

    第42回日本呼吸器学会中国四国地方会 

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    開催年月日: 2007年7月6日

    開催地:広島  

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  • 肺非小細胞癌における治療前血清KL-6値とゲフィチニブ単剤療法の治療効果の関連についての検討

    藤原義郎、木浦勝行、瀧川奈義夫、堀田勝幸、*宮原信明、谷本安、金廣有彦、加藤勝也、田端雅弘、谷本光音

    第42回日本呼吸器学会中国四国地方会 

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    開催年月日: 2007年7月6日

    開催地:広島  

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  • CD8T細胞およびロイコトリエンB4受容体の気道過敏性における役割の検討

    宮原信明、Christian Taube、武田勝行 、池田元洋1、渕本康子、古賀光、谷本安、金廣有彦、谷本光音、Erwin Gelfand

    日本アレルギー学会春季臨床大会 

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    開催年月日: 2007年6月10日

    会議種別:口頭発表(一般)  

    開催地:横浜  

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  • Corticosteriods enhace effector memory CD8T cell-mediated airway hyperresponsiveness and allergic airway inflammation by upregulating the leukotriene B4 receptor, BLT1

    H Ohnishi1, *N Miyahara1, CH Swasey1, K Takeda1, A Dakhama1, J Domenico1, JJ Lucas1, B Haribabu2, EW Gelfand1.

    103th ATS 2007 

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    開催年月日: 2007年5月22日

    開催地:San Francisco  

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  • Anti-IgE prevents respiratory syncytial virus (RSV)-specific IgE mediated mouse mast cell degranulation in vitro and development of enhanced airway hyperresponsiveness in vivo

    YM Lee, *N Miyahara, K Takeda, Balhorn A, A Joetham, EW Gelfand, Dakhama A

    103 ATS 

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    開催年月日: 2007年5月22日

    開催地:San Francisco  

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  • Requirement for the Leukotriene B4 Receptor-1 (BLT1) on Dendritic Cells in the Development of Allergen-Induced Airway Hyperresponsiveness

    Miyahara N, Matsuda H, Miyahara S, Takeda K, Koya T, Ohnishi H, Matsubara S, Okamoto M, Dakhama A, Haribabu B, and Gelfand EW

    103th American Thoracic Society (ATS) 2007 

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    開催年月日: 2007年5月22日

    開催地:San Francisco  

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  • Naturally occurring CD4+CD25+ regulatory T cells suppress CD8 T cell-mediated allergic airway hyperresponsiveness and inflammation.

    A Joetham, K Takeda, S Matsubara, N Miyahara, K Koya, H Onishi, A Dakhama, EW Gelfand

    103 ATS 

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    開催年月日: 2007年5月21日

    開催地:San Francisco  

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  • Timing of allergen sensitization with adoptively transdferred dendritic cell differentiate airway hyperresponsiveness and airway inflammation

    T Koya, K Takeda, H Matsubara, N Miyahara, EW Gelfand

    103 ATS 

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    開催年月日: 2007年5月21日

    開催地:San Francisco  

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  • Additive effect of montelukast and carbocysteine on airway hyperresponsiveness and airway inflammation

    Takeda K, Matsubara S, *Miyahara N, Matsuda H, Koya T, Ohnishi H, Okamoto M, Dakhama A, and Gelfand EW

    103 ATS 

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    開催年月日: 2007年5月21日

    開催地:San Francisco  

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  • Activation of invariant NKT cells with ligand loaded bone marrow derived dendritic cells in the initiation phase alters allergic airway inflammation and airway responsiveness

    H Matsuda, K Takeda, Koya T, *N Miyahara, M Okamoto, Dakhama A, and E.W. Gelfand EW.

    103 ATS 

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    開催年月日: 2007年5月21日

    開催地:San Francisco  

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  • Role of Fcgamma R3 in the maintenace phase of allergen-indeced airway hyperresponsiveness and airway inflammation

    K Takeda, A Hirano,*N Miyahara, Koya T, K Kitamura, A Kanehiro, T Tanimoto, M Harada, Dakhama A, and E.W. Gelfand EW.

    103 ATS 

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    開催年月日: 2007年5月21日

    開催地:San Francisco  

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  • Role of IFN-gamma in the development of airway hyperresponsiveness following RS virus infection in mice

    YM Lee, *N Miyahara, K Takeda, Balhorn A, A Joetham, EW Gelfand, Dakhama A

    103 ATS 

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    開催年月日: 2007年5月21日

    開催地:San Francisco  

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  • Essential role of V gamma TCR T cells in ozone-induced airway hyperresponsiveness

    S Matsubara, N Jin, A Joetham, K Takeda, *N Miyahara, T Koya, YM Lee, A Dakhama, EW Gelfand

    103 ATS 

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    開催年月日: 2007年5月21日

    開催地:San Francisco  

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  • The role of notch signaling in effector memory CD8 T cell development of airway hyperresponsiveness

    M. Okamotom, K Takeda, H. Onishi, H.Matsuda, S. Matsubara, N. Miyahara, A. Dakhama, EW. Gelfand.

    103th ATS 

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    開催年月日: 2007年5月20日

    開催地:San Francisco  

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  • 中年男性に発症したマイコプラズマ肺炎とクラミジア肺炎の重複感染

    久保寿夫, 瀧川奈義夫, 市原英基, 谷本 安, 田端雅弘, *宮原信明, 金廣有彦, 木浦勝行, 谷本光音

    第96回内科学会中国地方会 

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    開催年月日: 2007年5月19日

    開催地:岡山市  

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  • 高齢者の慢性甲状腺炎術後に発症したびまん性肺胞出血の1例

    藤井昌学, 宮原信明, 湯本哲也, 瀧川奈義夫, 谷本 安, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音

    第96回内科学会中国地方会 

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    開催年月日: 2007年5月19日

    開催地:岡山市  

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  • 早期に診断し得た肺ランゲルハンス細胞性組織球症の1例

    古賀 光, 谷本 安, 渊本康子, 大橋圭明, 宮原信明, 瀧川奈義夫, 田端雅弘, 金廣有彦, 木浦勝行, 片岡幹男, 谷本光音

    第16回日本呼吸器内視鏡学会中国四国支部会 2008.2.2(岡山) 

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    開催年月日: 2007年4月

    会議種別:口頭発表(一般)  

    開催地:第16回日本呼吸器内視鏡学会中国四国支部会 2008.2.2(岡山)  

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  • 経皮的心肺補助(PCPS)が有効であった移植後閉塞性細気管支炎によるCO2ナルコーシスの1例

    早稲田公一, 谷本 安, 宮原信明, 瀧川奈義夫, 田端雅弘, 金廣有彦, 木浦勝行, 谷本光音, (市場晋吾, 氏家良人)

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年4月

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • 進行副腎癌症例に対しOPEC療法を導入した長期生存の1例

    越智宣昭, 田端雅弘, 柏原宏美, 宮原信明, 瀧川奈義夫, 谷本 安, 金廣有彦, 木浦勝行, 谷本光音

    第97回日本内科学会中国地方会 2007.11.17(岡山) 

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    開催年月日: 2007年4月

    会議種別:口頭発表(一般)  

    開催地:第97回日本内科学会中国地方会 2007.11.17(岡山)  

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  • In vitro and in vivo effects of IL-10-treated dendritic cells on airway allergic inflammation

    Koya T, Takeda K, Matsubara S, *Miyahara N, , Swasey CH, Okamoto M, Dakhama A, and Gelfand EW.

    Amerian Academy of Allergy Asthma and Immunology (AAAAI). 

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    開催年月日: 2007年3月7日

    開催地:Miami beach. Florida  

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  • The Role of IL-13 in the Development of Allergic Rhinitis in Mice

    S. Miyahara, *N Miyahara, S. Matsubara, Anthony Joetham, and E. W. Gelfand

    AAAAI 

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    開催年月日: 2007年3月6日

    開催地:Miami Beach  

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  • CD8+/BLT1+/IL-13+ T cells in (Human) Asthma: Is There a Link to Steroid Resistance

    EW Gelfand, A Dakhama1, *N Miyahara1, S Wenzel, R Sutherland, E Goleva, RJ Martin, DY Leung

    AAAAI 

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    開催年月日: 2007年3月6日

    開催地:Miami beach  

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  • IL-10 is essential for naturally occurring lung CD4+CD25+T cell regulation of allergen-induced airway hyperresponsiveness

    Joetham AA, Takeda K, Shigeki M, *Miyahara N, Koya T, Dakhama A, and Gelfand EW

    AAAAI 

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    開催年月日: 2007年3月5日

    開催地:Miami beach  

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  • Importance of Both Allergen-Specific (ANR) and Non-Specific Nasal Reactivity (NNR) in the Development of Early- and Late-Phase Nasal Responses

    S. Miyahara, *N Myahara, S. Matsubara, Anthony Joetham, and E. W. Gelfand; Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO

    Amerian Academy of Allergy Asthma and Immunology 

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    開催年月日: 2007年2月12日

    開催地:San Diego  

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  • Activation of Effector Memory CD8+ T Cells Following Ligation of BLT1 by Leukotriene B4

    H Ohnishi1, *N Miyahara1, CH Swasey1, K Takeda1, A Dakhama1, J Domenico1, JJ Lucas1, B Haribabu2, EW Gelfand.

    Amerian Academy of Allergy Asthma and Immunology 

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    開催年月日: 2007年2月12日

    開催地:San Diego  

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  • Role of endogenous estrogen on airway hyperresponsiveness induced by allergen inhalation without adjuvant in female mice

    S Matsubara, CH Swasey, A Dakhama, JE Loader, H Ohnishi, A Joetham, A Balhorn, *N Miyahara, K Takeda, EW Gelfand

    Amerian Academy of Allergy Asthma and Immunology (AAAAI) 

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    開催年月日: 2007年2月12日

    開催地:San Diego  

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  • Importance of Both Allergen-Specific (ANR) and Non-Specific Nasal Reactivity (NNR) in the Development of Early- and Late-Phase Nasal Responses

    S. Miyahara, *N. Miyahara, S. Matsubara, A. Joetham and E.W. Gelfand

    AAAAI 

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    開催年月日: 2007年2月

    開催地:San Diego, USA  

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  • Activation of Effector Memory CD8+ T Cells Following Ligation of BLT1 by Leukotriene B4

    H. Ohnishi, N. Miyahara, C.H. Swasey, K. Takeda, A. Dakhama, J. Domenico, J.J. Lucas, S. Mathis, B. Haribabu and E.W. Gelfand

    Amerian Academy of Allergy Asthma and Immunology (AAAAI) 

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    開催年月日: 2007年2月

    開催地:San Diego, USA  

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  • Role of Endogenous Estrogen in Regulating Airway Hyperresponsiveness Induced by Allergen Inhalation Without Adjuvant

    S. Matsubara, C.H. Swasey, A. Dakhama, J.E. Loader, H. Ohnishi, A. Joetham, A. Balhorn, N. *Miyahara, K. Takeda and E.W. Gelfand

    AAAAI 

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    開催年月日: 2007年2月

    開催地:San Diego, USA  

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  • CD4+T Cells Are Required for the Functional Activation of CD8+T Cells and Airway Hyperresponsiveness and Allergic Inflammation

    T. Koya, MD, K. Takeda, MD, S. Matsubara, PhD, *N. Miyahara, MD, S. Miyahara, MD, C. Swasey, BS, A. Balhorn, BS, A. Joetham, BS, A. Dakhama, PhD, E.W. Gelfand, MD

    102th ATS 

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    開催年月日: 2006年5月23日

    開催地:San Diego  

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  • Fc Gamma Receptor IIb (Fc RIIb) Negatively Regulates Allergen-Induced Development of Airway Hyperresponsiveness and Inflammation in Mice

    K. Takeda, MD, *N. Miyahara, MD, S. Matsubara, PhD, T. Koya, MD, K. Kitamura, MD, A. Hirano, MD, A. Kanehiro, MD, M. Tanimoto, MD, T. Takai, A. Joetham, C. Taube, A. Dakhama, E.W. Gelfand, MD

    102th ATS 

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    開催年月日: 2006年5月23日

    開催地:San Diego  

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  • Immuno-Modulatory Effects of Ambroxol on Allergen-Induced Airway Hyperresponsiveness (AHR) and Inflammation in Mice

    K. Takeda, MD, PhD, *N. Miyahara, MD, PhD, S. Matsubara, PhD, C. Taube, MD, A. Balhorn, BS, A. Dakhama, PhD, K. Kitamura, MD, A. Hirano, MD, M. Tanimoto, MD,PhD, E.W. Gelfand, MD

    102th ATS 

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    開催年月日: 2006年5月23日

    開催地:San Diego  

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  • Leukotriene B4 Receptor (BLT1) Expression on Effector CD8+ TCells is Required for Mast Cell-Dependent Airway Hyperresponsiveness.

    *Miyahara N, Taube C, Takeda K, Miyahara S, Koya T, Loader J, Ott V, Swanson B, Shultz LD, Matsubara S, Tager AM, Luster AD, Dakhama A, Gelfand EW.

    102th Annual meeting of American Thoracic Society (ATS) 

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    開催年月日: 2006年5月22日

    開催地:San Diego  

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  • Confirmation of the Essential Role of Leukotriene B4 in the Development of Airway Hyperresponsiveness Using Leukotriene A4 Hydrolase-Deficient Mice.

    *Miyahara N, Miyahara S, Takeda K, Matsubara S, Koya T, Joetham A, Dakhama A, and E.W. Gelfand EW.

    102th ATS 

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    開催年月日: 2006年5月22日

    開催地:San Diego  

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  • The Role of CD44 in Established Allergic Airway Disease.

    *Miyahara N, Takeda K, Miyahara S, Matsubara S, Kodama T, Koya T, Dakhama A, and Gelfand EW.

    102th ATS 

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    開催年月日: 2006年5月22日

    開催地:San Diego  

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  • IL-10 Is Essential for the Immunoregulatory Function of Naturally-Occurring CD4+CD25+ T Cells in Allergen-Induced Airway Hyperresponsiveness and Inflammation

    A. Joetham, BS, K. Takeda, MD/PhD, S. Matsubara, PhD, *N. Miyahara, MD/PhD, T. Koya, MD/PhD, A. Dakhama, PhD, E.W. Gelfand, MD,

    102 ATS 

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    開催年月日: 2006年5月22日

    開催地:San Diego  

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  • Maternal Immunity Determines the Outcome of Neonatal Respiratory Syncytial Virus (RSV) Infection in the Offspring

    A. Dakhama, PhD, Y.M. Lee, MD, A. Balhorn, BSc, A. Joetham, BSc, *N. Miyahara, MD, T. Koya, MD, S. Matsubara, PhD, K. Takeda, MD, E.W. Gelfand, MD

    102th ATS 

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    開催年月日: 2006年5月22日

    開催地:San Diego  

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  • Infection with Influenza A Virus Does Not Mediate Airway Hyperresponsiveness nor Does It Alter the Response to Infection with RSV

    Y.M. Lee, MD, PhD, A. Balhorn, K. Takeda, MD, T. Koya, MD, *N. Miyahara, MD, A. Joetham, E.W. Gelfand, MD, PhD, A. Dakhama, PhD

    102th ATS 

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    開催年月日: 2006年5月22日

    開催地:San Diego  

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  • The Leukotriene B4 Receptor (BLT1) is Required for Effector CD8+ T-Cell-Mediated, Mast Cell-Dependent Airway Hyperresponsiveness.

    *Miyahara N, Taube C, Takeda K, Miyahara S, Koya T, Loader J, Ott V, Swanson B, Shultz LD, Matsubara S, Tager AM, Luster AD, Dakhama A, Gelfand EW.

    Amerian Academy of Allergy Asthma and Immunology (AAAAI). 

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    開催年月日: 2006年3月6日

    開催地:Miami beach. Florida  

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  • Combination of interleukin (IL)-2 and IL-18 attenuates allergen-induced airway hyperresponsiveness (AHR) and inflammation through an IL-12-STAT4-interferon (IFN)-gamma pathway

    Matsubara S, Takeda K, Kodama T,*Miyahara N, Koya T, Dakhama A, and Gelfand EW

    Amerian Academy of Allergy Asthma and Immunology (AAAAI). 

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    開催年月日: 2006年3月6日

    開催地:Miami beach. Florida  

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  • The Role of IL-13 in the Development of Allergic Rhinitis in Mice

    S. Miyahara, *N. Miyahara, S. Matsubara, T. Koya, K. Takeda and E.W. Gelfand

    AAAAI 

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    開催年月日: 2006年3月1日

    開催地:San Antonio, TX, USA  

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  • IL-10 Is Essential For Naturally Occurring Lung CD4+CD25+ T Cell Regulation of Allergen-induced Airway Hyperresponsiveness

    A.A. Joetham, K. Takeda, M. Shigeki, C. Taube, N. *Miyahara, T. Koya, A. Dakhama and E. Gelfand

    Amerian Academy of Allergy Asthma and Immunology (AAAAI) 

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    開催年月日: 2006年3月1日

    開催地:San Antonio, TX, USA  

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  • In Vitro and in Vivo Effects of IL-10-Treated Dendritic Cells on Airway Allergic Inflammation

    T. Koya, K. Takeda, S. Matsubara, *N. Miyahara, S. Miyahara, C. Swasey, A. Barhorn, A. Joetham, A. Dakhama and E.W. Gelfand

    AAAAI 

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    開催年月日: 2006年3月1日

    開催地:San Antonio, TX, USA  

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  • Combination of Interleukin (IL)-2 and IL-18 Attenuates Allergen-Induced Airway Hyperresponsiveness (AHR) and Inflammation through An IL-12-STAT4-Interferon (IFN)-gamma Pathway

    S. Matsubara, K. Takeda, T. Kodama, T. Koya, *N. Miyahara, A. Joetham, C.H. Swasey, A. Dakhama and E.W. Gelfand

    AAAAI 

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    開催年月日: 2006年3月1日

    開催地:San Antonio, TX, USA  

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  • CD4+CD25+ T Cells from Sensitized/Challenged Lung Regulate Allergen-Induced Airway Hyperresponsiveness and Inflammation in Mice

    A. Joetham, BS, C. Taube, MD, K. Takeda, MD/PhD, *N. Miyahara, MD/PhD, A. Dakhama, PhD, E.W. Gelfand, MD

    101th American Thoracic Society (ATS) 2005 San Diego, CA 

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    開催年月日: 2005年5月24日

    開催地:San Diego  

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  • Essential Role of Fc Receptorγ Chain for Antigen-Presentation in Development of Airway Hyperresponsiveness (AHR) and Allergic Airway Inflammatio

    K. Takeda, MD, K. Kitamura, MD, *N. Miyahara, MD, T. Kodama, MD, T. Koya, MD, A. Hirano, MD, A. Kanehiro, MD, T. Takai, PhD, M. Tanimoto, MD, M. Harada, MD, C. Taube, A. Dakhama, E.W. Gelfand, MD

    101th ATS 

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    開催年月日: 2005年5月24日

    開催地:San Diego  

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  • Liposome Antigen Nucleic Acid Vaccine Modulates Airway Hyperresponsiveness and Airway Inflammation in Mice by Expansion of Antigen Specific CD8+ T Cells

    K. Takeda, MD, S.W. Dow, DVM, *N. Miyahara, MD, K. Kodama, MD, C. Taube, MD, A. Joetham, A. Balhorn, A. Dakhama, PhD, R.M. Kedl, PhD, E.W. Gelfand, MD

    101th ATS 

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    開催年月日: 2005年5月24日

    開催地:San Diego  

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  • Inhibitory Action of a Specific Syk Kinase Inhibitor on Allergen-Induced Airway Hyperresponsiveness and Inflammation in Mice

    S. Matsubara, PhD, K. Takeda, MD, G. Li, MD, T. Koya, MD, *N. Miyahara, MD, J.E. Loader, A. Joetham, P. Pine, PhD, J.J. Lucas, PhD, E.W. Gelfand, MD, Denver, CO

    101th ATS 

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    開催年月日: 2005年5月24日

    開催地:San Diego  

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  • Role of CD4 and CD8 T Cells in the Enhancement and Prevention of Airway Hyperresponsiveness (AHR) Following Re-Infection with Respiratory Syncytial Virus (RSV)

    Dakhama, PhD, M. El Gazzar, PhD, A. Joetham, BSc, A. Balhorn, BSc, *N. Miyahara, MD, K. Takeda, MD, E.W. Gelfand, MD

    101th ATS 

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    開催年月日: 2005年5月24日

    開催地:San Diego  

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  • Na&iuml;ve (Non-Primed) CD4+CD25+ T Regulatory Cells Suppress Allergic Airway Hyperresponsiveness in an Antigen-Independent Manner

    A. Joetham, BS, K. Takeda, MD/PhD, *N. Miyahara, MD/PhD, A. Balhorn, BS, A. Dakhama, PhD, E.W. Gelfand, MD

    101th ATS 

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    開催年月日: 2005年5月24日

    開催地:San Diego  

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  • The Leukotriene B4 Receptor-1 (BLT1) is Essential for Allergen-Mediated Recruitment of CD8+ T Cells and Induction of Airway Hyperresponsiveness.

    Nobuaki Miyahara, Katsuyuki Takeda, Satoko Miyahara, Anthony Joetham, Christian Taube, Toshiyuki Koya, Shigeki Matsubara, Azzeddine Dakhama, Andrew M. Tager, Andrew D. Luster, and Erwin W. Gelfand.

    101th ATS 2005 San Diego, CA 

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    開催年月日: 2005年5月24日

    開催地:San Diego, CA  

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  • CC Chemokine Ligand 5 (RANTES) Regulates Airway Function Following Repeated Antigen Challenge in Mice

    T. Koya, M.D., K. Takeda, M.D., T. Kodama, M.D., *N. Miyahara, M.D., S. Matsubara, Ph.D., A. Joetham, A. Balhorn, A. Dakhama, Ph.D., E.W. Gelfand, M.D

    101th ATS 

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    開催年月日: 2005年5月23日

    開催地:San Diego  

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  • Role of G1-Phase Cyclin Dependent Kinases (Cdks) and D-Type Cyclins in Growth and Differentiation of CD8+ T Effector and T Central Memory Cell

    T.N. Lively, PhD, *N. Miyahara, MD/PhD, J. Domenico, BS, J.J. Lucas, PhD, E.W. Gelfand, MD

    101th ATS 

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    開催年月日: 2005年5月23日

    開催地:San Diego  

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  • The Role of The High Affinity IgE Receptor in Allergic Rhinitis in Mice

    Satoko Miyahara, Nobuaki Miyahara, Katsuyuki Takeda, Shigeki Matsubara and Erwin W. Gelfand

    Amerian Academy of Allergy Asthma and Immunology (AAAAI) 

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    開催年月日: 2005年3月1日

    開催地:San Antonio, TX, USA  

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  • Complement activation through the alternative pathway is necessary for the development of airway hyperresponsiveness (AHR) and inflammation in a model of human asthma

    Thurman JM, Taube C, Takeda K, *Miyahara N, Kodama T, Rha Y, Joetham A, Balhorn A, Swasey C, Dakhama A, Giclas PC, Gelfand EW, Holers VM

    MOLECULAR IMMUNOLOGY 

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    開催年月日: 2004年6月24日

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  • Kinetics of Cytokine Production with Repeated Allergen Exposure in Sensitized Mice

    Taku Kodama, Katsuyuki Takeda, *Nobuaki Miyahara, Eun-Seok Yang, Chistian Taube, Anthony Joetham, Azzedine Dakhama, Jung-Won Park, ErwinW. Gelfand

    100th ATS 

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    開催年月日: 2004年5月26日

    開催地:Orland  

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  • Age at First Infection Determines the Phenotype of Airway Response to Re-Infection by Respiratory Syncytial Virus (RSV) in Mice

    A. Dakhama, J.W. Park, C. Taube, A. Joetham, A. Balhorn, *N. Miyahara, T. Kodama, K. Takeda, E.W. Gelfand

    100th ATS 

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    開催年月日: 2004年5月26日

    開催地:Orland  

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  • The High-Affinity IgE Receptor (Fc RI) Is Necessary for the Development of Airway Hyperresponsiveness (AHR) Following Sensitization without Adjuvant

    Taube, A. Joetham, K. Takeda, *N. Miyahara, T. Kodama, C. Swasey, A. Balhorn, A. Dakhama, E.W. Gelfand

    100th ATS 

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    開催年月日: 2004年5月25日

    開催地:Orland  

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  • Liposome Antigen Nucleic Acid Vaccine (LANAC) Modulates Airway Hyperresponsiveness and Airway Inflammation in Mice by Expansion of INF- Secreting Tetramer Positive Cells in the Lung

    K. Takeda, S.W. Dow, N. Miyahara, T. Kodama, C. Taube, A. Balhorn, J.W. Park, R.M. Kedl, E.W. Gelfand

    100th ATS 

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    開催年月日: 2004年5月25日

    開催地:Orland  

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  • Defective Primary and Secondary/Memory CD8+T Cell Responses in the Absence of CD4+T Cells Following Sensitization to Allerge

    A. Joetham, C. Taube, K. Takeda, *N. Miyahara, A. Balhorn, Z.H. Cui, A. Dakhama, E.W. Gelfand

    100th ATS 

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    開催年月日: 2004年5月25日

    開催地:Orland  

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  • Complement Activation through the Alternative Pathway Is Necessary for the Development of Airway Hyperresponsiveness (AHR) and Inflammation

    C. Taube, J.M. Thurman, K. Takeda, T. Kodama, *N. Miyahara, Y.H. Rha, A. Joetham, A. Balhorn, C. Swasey, A. Dakhama, P.C. Giclas, V.M. Holers, E.W. Gelfan

    100th ATS 

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    開催年月日: 2004年5月25日

    開催地:Orland  

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  • Overexpression of Surfactant Protein D (SP-D) Inhibits Airway Hyperresponsiveness and Airway Inflammation in Mice by Up-Regulating Th-1 Cytokines in the Lung

    K. Takeda, J.H. Fisher, *N. Miyahara, T. Kodama, C. Swasey, A. Joetham, A. Balhorn, C. Taube, A. Dakhama, D.R. Voelker, R.J. Mason, E.W. Gelfand

    100th ATS 

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    開催年月日: 2004年5月24日

    開催地:Orland  

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  • Respiratory Syncytial Virus (RSV)-Induced Airway Hyperresponsiveness (AHR) Is Associated with Altered Airway Sensory Neuropeptide Expression in Mice

    A. Dakhama, J.W. Park, C. Taube, A. Balhorn, A. Joetham, *N. Miyahara, T. Kodama, K. Takeda, J.E. Loader, G.L. Larsen, E.W. Gelfan

    100th ATS Orland 

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    開催年月日: 2004年5月23日

    開催地:Orland  

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  • Physiological Assessment of Allergic Rhinitis in Mice.

    Satoko Miyahara, *Nobuaki Miyahara, Katsuyuki Takeda, Annette Balhorn, Christina Swasey, and Erwin W. Gelfand.

    100th ATS 

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    開催年月日: 2004年5月22日

    開催地:Orlando, Florida  

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  • Kinetic Analysis of Oral Tolerance Following Development of Allergen-Induced Airway Hyperresponsiveness in Mice.

    *Nobuaki Miyahara, Katsuyuki Takeda, Taku Kodama, Satoko Miyahara, Anthony Joetham, Christian Taube, Azzeddine Dakhama, and Erwin W. Gelfand

    100th American Thoracic Society (ATS) 2004 

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    開催年月日: 2004年5月22日

    開催地:Orlando, Florida  

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  • 呼吸器疾患のMolecular~Clinical Physiology 招待

    第60回 東京医科歯科大学呼吸器内科同門会  2022年1月22日 

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▼全件表示

受賞

  • 岡山医学会賞(砂田賞)

    2021年   岡山医学会  

    小田尚廣, 宮原信明

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  • American Thoracic Society, travel award

    2007年   American Thoracic Society  

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  • American Academy of Allergy Asthma and Immunology STAR Program Award

    2006年   米国アレルギー学会  

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共同研究・競争的資金等の研究

  • 呼吸器疾患とバイオマーカーに関する前向き観察研究

    2021年11月

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  • 肺の各部位における分子生物学的特徴に関する研究

    2021年11月

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  • 重症喘息に対する生物学的製剤使用実態に関する後ろ向き観察研究

    2021年11月

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    担当区分:研究代表者 

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  • ケモカイン抑制能を強化した新規間葉系幹細胞による慢性閉塞性肺疾患の細胞療法開発

    研究課題/領域番号:21K08155  2021年04月 - 2025年03月

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    宮原 信明, 中山 享之, 谷口 暁彦

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    担当区分:研究代表者  資金種別:競争的資金

    配分額:4030000円 ( 直接経費:3100000円 、 間接経費:930000円 )

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  • ニューモシスティス肺炎の予後に関する因子の検討のための多施設共同後ろ向き観察研究

    2021年04月

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  • 睡眠ポリグラフ検査との比較による腕時計型活動量計の機能評価

    2021年03月

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  • 多分野合議による間質性肺炎診断に対する多施設共同前向き観察研究 Providing Multidisciplinary ILD diagnoses (PROMISE) study

    2021年01月 - 2023年03月

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    担当区分:研究代表者  資金種別:産学連携による資金

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  • 通信型サーマルセンサーによる客観的Performance Statusの創出

    2020年06月

    介入研究

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    担当区分:研究分担者  資金種別:産学連携による資金

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  • 薬剤性肺障害の診断や予後予測とFeNOの相関性の解析

    2020年05月

    観察研究

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    担当区分:研究分担者 

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  • 新規SP-D測定試薬の性能評価

    2020年03月 - 2021年05月

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    担当区分:研究分担者  資金種別:産学連携による資金

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  • 希少な呼吸器疾患の診療実態及び治療の有用性を明らかにするための前向き観察研究 (CS-Lung Rare)

    2020年

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    担当区分:研究分担者 

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  • 気管支拡張症合併難治性喘息の実態調査

    2020年

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    担当区分:研究分担者 

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  • 重症喘息患者の増悪予測因子に関する前向き観察研究 ―岡山重症喘息プログラム(Okayama-SARP)―

    2020年

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    担当区分:研究代表者 

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  • 間質性肺炎のNeuropeptide Y (NPY)による免疫応答を介した肺の線維化メカニズムに関する病態研究

    2019年09月

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    担当区分:研究代表者  資金種別:産学連携による資金

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    担当区分:研究分担者 

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    2019年07月

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    担当区分:研究分担者 

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    担当区分:研究分担者  資金種別:産学連携による資金

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    2018年06月

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    担当区分:研究分担者 

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    2018年05月