研究者詳細 - 宮原　信明

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Pulmonary epithelioid haemangioendothelioma mimicking lung cancer. 査読国際誌

Naohiro Oda, Yoshinobu Maeda, Kastuyuki Kiura, Nobuaki Miyahara

BMJ case reports 14 ( 2 ) 2021年2月

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

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

記述言語：英語掲載種別：学位論文（博士）

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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A Case of Lung Cancer That Showed an Abscopal Effect after Irradiation of Simultaneous Oropharyngeal Cancer

Kayo Nakamura, Eiki Ichihara, Yusaku Shibata, Etsuko Murakami, Nobuaki Miyahara, Daizo Kishino

Japanese Journal of Lung Cancer 91 ( 2 ) 109 - 112 2021年

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：Japan Lung Cancer Society

Background. The abscopal effect is a phenomenon in which tumor shrinkage occurs outside the radiation field. It usually occurs between the primary tumor and metastatic lesions of the same cancer or between metastatic lesions, and there have been no reports on the abscopal effect occurring after irradiation of other cancer types. Case. A woman in her 50s was diagnosed with double primary cancer of lung and oropharyngeal cancer. After the administration of nivolumab as second-line treatment for lung cancer, the lung cancer did not show any increase in size for six months (stable disease). However, the pharyngeal cancer showed progression, so irradiation was started for it. After radiotherapy, shrinkage of the primary lung cancer (outside the irradiation field) was observed. Conclusion. We experienced a case in which primary lung cancer shrank after irradiation for primary pharyngeal cancer. This case suggests that abscopal-like effects may occur between different cancer types.

DOI： 10.2482/HAIGAN.61.109

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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. 査読国際誌

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

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. 査読国際誌

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

担当区分：責任著者記述言語：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.

DOI： 10.1371/journal.pone.0236935

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[The role of neuropeptide Y for the development of allergic airway responses]. 招待査読

Nobuaki Miyahara

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

担当区分：筆頭著者,　最終著者,　責任著者記述言語：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

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

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

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

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

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

記述言語：英語掲載種別：学位論文（博士）

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.

DOI： 10.1186/s12931-018-0963-0

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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

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

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

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

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

担当区分：責任著者記述言語：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.

DOI： 10.18926/AMO/55446

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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

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.

DOI： 10.1016/j.resinv.2017.03.002

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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

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.

DOI： 10.2147/COPD.S133071

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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

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.

DOI： 10.1186/s12931-017-0507-z

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論文 - 宮原　信明