Updated on 2022/11/02

写真a

 
YOKOTA Kenji
 
Organization
Faculty of Health Sciences Professor
Position
Professor
Profile
昭和62年4月1日 研究生 札幌医科大学微生物学講座
平成4年7月1日 助手 岡山大学医学部細菌学講座
平成10年7月1日 同講師
平成11年7月16日 講師 岡山大学大学院医歯学総合研究科 (Dマル合教員)
平成17年4月1日 助教授 岡山大学医学部保健学科
平成20年4月1日 准教授 岡山大学大学院保健学研究科
平成28年4月1日 同教授
感染症学会評議員
ヘリコバクター学会代議員(耐性菌パネル委員)
External link

Degree

  • 医学博士 ( 1999.6   岡山大学 )

Research Areas

  • Life Science / Bacteriology

Education

  • Okayama University   医学部  

    - 1997.6

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    Notes: 医学博士

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Research History

  • Okayama University   Graduate School of Health Sciences   Professor

    2015.4

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  • Okayama University   Graduate School of Health Sciences   Associate Professor

    2005.4 - 2015.3

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  • Okayama University   Graduate School of Medicine , Dentistry and Pharmaceutical Sciences   Lecturer

    1998.7 - 2005.3

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  • Okayama University   Medical School   Research Assistant

    1992.8 - 1998.6

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  • Sapporo Medical University   微生物学講座

    1987.4 - 1992.6

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Papers

  • Elizabethkingia anophelis, an emerging pathogen, inhibits RAW 264.7 macrophage function. International journal

    I Putu Bayu Mayura, Kazuyoshi Gotoh, Hayato Nishimura, Erina Nakai, Takehiko Mima, Yumiko Yamamoto, Kenji Yokota, Osamu Matsushita

    Microbiology and immunology   65 ( 8 )   317 - 324   2021.8

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    Elizabethkingia anophelis is a pathogen that can cause a life-threatening infection in immunocompromised patients. The first case of E. anophelis infection was reported in 2013; subsequently, an increase in its incidence has been reported globally. Additionally, a mortality rate of more than 30% was observed in the US outbreak of 2015. To date, the pathogenic mechanisms underlying E. anophelis infection, such as toxin production, remain unclear. Since tissue macrophages act as the first line of defense against pathogens, in the present study the interactions between E. anophelis and a macrophage-like cell line RAW 264.7 were examined. Although E. anophelis showed no cytotoxicity toward RAW 264.7 macrophages, the infection inhibited LPS-induced morphological changes and activation of differentiation markers for the polarization of RAW 264.7 macrophages toward an M1-like phenotype. However, when the cell contact was restricted using Transwell inserts or bacterial culture supernatants were used instead of live bacteria, no such inhibition was observed. Moreover, it was shown that E. anophelis evaded phagocytosis. Overall, the results suggest that E. anophelis infection inhibits the differentiation of RAW 264.7 macrophages to a pro-inflammatory phenotype in a contact-dependent manner.

    DOI: 10.1111/1348-0421.12888

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  • Serodiagnosis and bacterial genome of helicobacter pylori infection

    Aina Ichihara, Hinako Ojima, Kazuyoshi Gotoh, Osamu Matsushita, Susumu Take, Hiroyuki Okada, Akari Watanabe, Kenji Yokota

    Toxins   13 ( 7 )   2021.7

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    The infection caused by Helicobacter pylori is associated with several diseases, including gastric cancer. Several methods for the diagnosis of H. pylori infection exist, including endoscopy, the urea breath test, and the fecal antigen test, which is the serum antibody titer test that is often used since it is a simple and highly sensitive test. In this context, this study aims to find the association between different antibody reactivities and the organization of bacterial genomes. Next-generation sequences were performed to determine the genome sequences of four strains of antigens with different reactivity. The search was performed on the common genes, with the homology analysis conducted using a genome ring and dot plot analysis. The two antigens of the highly reactive strains showed a high gene homology, and Western blots for CagA and VacA also showed high expression levels of proteins. In the poorly responsive antigen strains, it was found that the inversion occurred around the vacA gene in the genome. The structure of bacterial genomes might contribute to the poor reactivity exhibited by the antibodies of patients. In the future, an accurate serodiagnosis could be performed by using a strain with few gene mutations of the antigen used for the antibody titer test of H. pylori.

    DOI: 10.3390/toxins13070467

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  • カルバペネマーゼ産生腸内細菌科細菌に対するビアペネムの殺菌効果

    三好 諒, I Putu Bayu Mayura, 後藤 和義, 美間 健彦, 山本 由弥子, 横田 憲治, 松下 治, 萩谷 英大

    日本細菌学雑誌   76 ( 1 )   119 - 119   2021.2

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  • Antibacterial effects of disulfiram in helicobacter pylori

    Tomomi Kobatake, Keiki Ogino, Hiroyuki Sakae, Kazuyoshi Gotoh, Akari Watanabe, Osamu Matsushita, Hiroyuki Okada, Kenji Yokota

    Infection and Drug Resistance   14   1757 - 1764   2021

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    Background: Helicobacter pylori infection poses a risk of the occurrence of gastrointestinal diseases, such as gastric cancer. Its incidence rate is significantly reduced by eradication, and thereby, eradication therapy is generally performed. Disulfiram is an oral prescription drug mainly used for the treatment of alcohol dependence. In recent years, reports have been made on its anticancer and antibacterial effects, and thus, it has recently become an interesting subject. This study aimed to examine the antibacterial activity of disulfiram, investigate the presence or absence of its antibacterial activity on H. pylori, and determine whether it could be a new bactericidal drug against drug-resistant H. pylori. Materials and Methods: Drug-sensitive strains of H. pylori and amoxicillin-resistant, clarithromycin-resistant, and metronidazole-resistant strains were used, and a growth inhibition test of H. pylori using disulfiram was performed. Furthermore, the expression of urease, vacuolating cytotoxin A (VacA), and CagA, the virulence proteins of H. pylori, was quantitatively analyzed using the Western blotting method. In addition, for H. pylori used in this study, the 16SrDNA sequence, a ribosomal gene involved in protein production, was analyzed to examine the presence or absence of gene mutation. Results: Disulfiram suppressed the growth of 7 out of 12 H. pylori strains at 1 µg/mL, and no correlation was observed between their susceptibility/resistance to current eradication antimicrobial drugs and disulfiram resistance. Disulfiram reduced the expression levels of urease, VacA, and CagA proteins. H. pylori, which showed resistance to disulfiram, tended to have fewer gene deletions/insertions in the 16S rDNA sequence; however, no specific mutation was detected. Conclusion: Disulfiram has a bactericidal effect on H. pylori at low concentrations, suggesting that it can be used as a supplement for current H. pylori eradication drugs.

    DOI: 10.2147/IDR.S299177

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  • Environmental survey of Methicillin-Resistant Staphylococci in a Hospital in Japan.

    Akari Watanabe, Tokiko Watanabe, Susumu Kokeguchi, Yumiko Yamamoto, Osamu Matsushita, Kenji Yokota

    Biocontrol science   26 ( 3 )   137 - 145   2021

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    We examined the hospital-wide incidence of methicillin-resistant Staphylococcus contamination in a hospital environment to predict the risk of the nosocomial spread of infection. Samples were also taken different surfaces and medical equipment in a general hospital ward and a staff station. The isolates were identified bacterial strains and analyzed by PCR for detection of the mecA gene and staphylococcal cassette chromosome mec (SCCmec) types (I-V). Overall, out of 146 isolates that were screened, 15.7% of the samples in the hospital wards were contaminated with Staphylococcus aureus and 74.7% were isolated with coagulase-negative Staphylococci (CNS). The methicillin-resistant mecA gene was detected in all oxacillin-resistant S. aureus, and 89% of oxacillin-resistant CNS was identified as methicillin-resistant S. aureus (MRSA) and MRCNS respectively. All S. aureus and CNS from the hospital wards with MRSA patients were detected as MRSA and MRCNS. A widespread distribution of MRSA and MRCNS was detected in the Cuff. The majority of the MRSA and MRCNS isolates in this study were SCCmec type V, which are a community-acquired infection type. The increased incidence and prevalence of community-acquired MRSA and MRCNS, as well as hospital-acquired MRSA, should be recognized as serious healthcare problems.

    DOI: 10.4265/bio.26.137

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  • 尿沈渣標本中に出現する顆粒状物質と尿路細菌叢との関連について

    佐藤 妃映, 横田 憲治, 渡辺 朱理, 苔口 進, 衛藤 友美, 高阪 翔士

    日本防菌防黴学会誌   48 ( 12 )   623 - 628   2020.12

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    健常人の尿沈渣標本中に,ステルンハイマー染色にて青色の顆粒状物質が出現することがある。この物質の成分や出現背景等に関して詳細は明らかとなっていないため,検討を行った。その結果,顆粒状物質は,健常な女性15名中8名(53%)に出現していた。SDS-PAGEによる電気泳動では,15名中11名(73%)に75KDaの単一のバンドを認め,質量分析にてTamm-Horsfall protein(THP)(Uromodulin)と同定された。THPは尿路細菌叢が存在した10名中9名(90%)で検出され,尿路に細菌や真菌が存在しなかった4名中3名(75%)では検出されなかった。また,顆粒状物質が出現していた8名中,THPと尿路細菌叢の両方を認めたのは4名(50%)であった。明らかな傾向を統計学的に証明できなかったが,顆粒状物質は,THPや尿路細菌叢と同時に検出される場合があることから,何らかの自然免疫学的な応答に関与している可能性が示された。今後,検体採取条件を再検討し,この関連性について検証する必要がある。(著者抄録)

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  • Risk of gastric cancer in the second decade of follow-up after Helicobacter pylori eradication. Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Chiaki Kusumoto, Takayuki Imada, Fumihiro Hamada, Tomowo Yoshida, Kenji Yokota, Toshiharu Mitsuhashi, Hiroyuki Okada

    Journal of gastroenterology   55 ( 3 )   281 - 288   2020.3

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    BACKGROUND AND AIMS: Eradication of Helicobacter pylori reduces the risk of gastric cancer. In this study, we investigated the risk beyond 10 years after eradication of H. pylori. METHODS: We conducted a retrospective cohort study of 2737 patients who had yearly endoscopic follow-up after cure of H. pylori infection. For comparison of gastric cancer risk in the second decade of follow-up with that in the first decade, we calculated standardized incidence ratios (SIRs) by dividing the number of observed cases of gastric cancer in the second decade of follow-up by that of expected cases which was estimated using the incidence rate ratio of age in the first decade. RESULTS: During the follow-up for as long as 21.4 years (mean 7.1 years), gastric cancer developed in 68 patients (0.35% per year). The SIRs for diffuse-type gastric cancer was infinity (0 expected case and 4 observed cases) in patients with mild gastric mucosal atrophy and 10.9 (95% confidence interval 4.53-26.1) with moderate atrophy, whereas no significant increase of SIRs was observed in intestinal-type cancer regardless of the grade of baseline gastric atrophy or in diffuse-type cancer in patients with severe atrophy even though who had the highest risk. CONCLUSIONS: The longer the follow-up, the greater the risk of developing diffuse-type gastric cancer becomes in patients with mild-to-moderate gastric atrophy at baseline. Endoscopic surveillance should be continued beyond 10 years after cure of H. pylori irrespective of the severity of gastric atrophy.

    DOI: 10.1007/s00535-019-01639-w

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  • Correction to: Risk of gastric cancer in the second decade of follow-up after Helicobacter pylori eradication. Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Chiaki Kusumoto, Takayuki Imada, Fumihiro Hamada, Tomowo Yoshida, Kenji Yokota, Toshiharu Mitsuhashi, Hiroyuki Okada

    Journal of gastroenterology   55 ( 3 )   289 - 290   2020.3

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    In the original publication of the article, the figure 3 was published with errors. The corrected figure 3 should appear as in this correction.

    DOI: 10.1007/s00535-019-01654-x

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  • Hepatic Campylobacter jejuni infection in patients with Castleman-Kojima disease (idiopathic multicentric Castleman disease with thrombocytopenia, anasarca, fever, reticulin fibrosis, and organomegaly (TAFRO) syndrome). International journal

    Chihiro Kageyama, Takuro Igawa, Yuka Gion, Noriko Iwaki, Tetsuya Tabata, Takehiro Tanaka, Eisei Kondo, Hajime Sakai, Koichi Tsuneyama, Kazuhiro Nomoto, Hiroko Noguchi, Tadashi Yoshino, Kenji Yokota, Yasuharu Sato

    Pathology international   69 ( 10 )   572 - 579   2019.10

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    Castleman-Kojima disease, also known as idiopathic multicentric Castleman disease with TAFRO syndrome (iMCD-TAFRO), is a recently recognized systemic inflammatory disorder with a characteristic series of clinical symptoms, including thrombocytopenia (T), anasarca (A), fever (F), reticulin fibrosis (R), and organomegaly (O). Patients with iMCD-TAFRO often develop severe abdominal pain, elevated alkaline phosphatase levels, and systemic inflammation, but the etiological factors are unknown. To investigate the potential role of bacterial infection in the pathogenesis of iMCD-TAFRO, we performed polymerase chain reaction (PCR) for the bacterial 16S rRNA gene with DNA extracted from liver specimens of three patients with iMCD-TAFRO, four patients with amyotrophic lateral sclerosis, and seven patients with inflammatory conditions. Sequencing of the PCR product showed 99% DNA sequence identity with Campylobacter jejuni in all three patients with iMCD-TAFRO and in two patients with inflammatory conditions. Immunohistochemical and electron microscopy analyses could not identify C. jejuni in patients with iMCD-TAFRO. The findings indicated that C. jejuni infection is not the pathological cause of iMCD-TAFRO; however, this ubiquitous bacterium may play a role in uncontrolled systemic hypercytokinemia, possibly through the development of cross-reactive autoantibodies.

    DOI: 10.1111/pin.12856

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  • 地域在住高齢者におけるメチシリン耐性ブドウ球菌の保菌状況調査

    渡辺 朱理, 横田 憲治, 林 俊治, 苔口 進

    日本環境感染学会総会プログラム・抄録集   34回   [P - 005]   2019.2

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  • A survey of Lasioderma serricorne (Fabricius) in Japanese Dental Clinics.

    Akari Watanabe, Satoru Takaku, Kenji Yokota, Shunji Hayashi, Naofumi Tamaki, Susumu Kokeguchi

    Biocontrol science   24 ( 2 )   117 - 121   2019

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    This study was to survey the capturing rate in Japanese dental clinics of the Lasioderma serricorne (cigarette beetles) , and to evaluate the beetle's potential as a carrier for transmission of nosocomial pathogens. L. serricorne imagoes were captured in pheromone traps in 14 Japanese dental clinics in August and September 2012 and 2013, and their numbers recorded. Polymerase chain reaction (PCR) for the bacterial antibiotic-resistant genes mecA, vanA, vanB, blaIMP, and blaVIM was performed on the captured L. serricorne imagoes. Bacterial species in the captured specimens were identified by 16S rRNA PCR and sequencing analysis. The L. serricorne imagoes were captured from 10 dental clinics (71.4%) . We failed to detect the presence of nosocomial antibiotic-resistant pathogens in L. serricorne imagoes. The bacterial species detected most commonly in the imagoes was Wolbachia sp., an intracellular proteobacterium infecting certain insect species. Monitoring of insects including L. serricorne should be incorporated into regiment of the infection control.

    DOI: 10.4265/bio.24.117

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  • Increase in antibiotic resistant Helicobacter pylori in a University Hospital in Japan. International journal

    Chihiro Kageyama, Mayu Sato, Hiroyuki Sakae, Yuka Obayashi, Yoshiro Kawahara, Takehiko Mima, Osamu Matsushita, Kenji Yokota, Motowo Mizuno, Hiroyuki Okada

    Infection and drug resistance   12   597 - 602   2019

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    Background: Eradication effectively prevents Helicobacter pylori-associated diseases; however, H. pylori antibiotic resistance has increased throughout Japan and worldwide. This study aimed to assess rates of resistance to antibiotics; amoxicillin, clarithromycin and metronidazole in a University Hospital in Japan. Materials and methods: H. pylori (208 strains) were isolated from patients at the Okayama University Hospital in Japan. The minimum inhibitory concentrations (MIC) were determined using the mean values of the E-test to determine the antimicrobial susceptibilities of the strains. Sequencing and gene analysis were performed to analyze resistance genes to clarithromycin and amoxicillin. Results: Rates of amoxicillin, clarithromycin, and metronidazole resistance were 13%, 48%, and 49%, respectively. Genetic analysis indicated that the A2143G point mutation in 23S rDNA is closely associated with the MIC of clarithromycin. The MIC in amoxicillin-resistant strains increased with an increase in the number of PBP1A amino acids mutations. Conclusion: Genetic analysis for resistant strains is not clinically effective in cases of amoxicillin resistance. Numerous bacteria with already high antibiotic resistance rates have been isolated in large hospitals such as a University Hospital. For effective eradication therapy, MIC measurement should be considered via several methods.

    DOI: 10.2147/IDR.S196452

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  • Association of host immunity with Helicobacter pylori infection in recurrent gastric cancer. International journal

    Mayu Sato, Kou Miura, Chihiro Kageyama, Hiroyuki Sakae, Yuka Obayashi, Yoshiro Kawahara, Osamu Matsushita, Kenji Yokota, Hiroyuki Okada

    Infectious agents and cancer   14   4 - 4   2019

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    Background: Helicobacter pylori infection is associated with the incidence of gastric cancer. Endoscopic resection has been developed as a proper technique to treat early stage of gastric cancer. However, some patients develop recurrent gastric cancer within 5 years after endoscopic treatment. The aim of the present study is to explore a biomarker for detecting people who has high risk of gastric cancer recurrence. Methods: We analyzed the Interleukin-10 (IL-10) single nucleotide polymorphism (SNP) and IgG subclass responses to the bacteria in patients with early gastric cancer and recurrent gastric cancer. Results: Patients with hetero-type in the 1082 SNP and CC genotype in the 592 SNP were at high risk of recurrence of gastric cancer. In patients with genotype carrying high risk of recurrence, IgG1 level tended to be higher than that in patients with other genotypes. Conclusions: Dominance of T helper 2 (Th2) immunity controlled by IL-10 cytokine may be associated with H. pylori-associated gastric cancer recurrence.

    DOI: 10.1186/s13027-019-0221-1

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  • Use of ATP bioluminescence to survey the spread of aerosol and splatter during dental treatments Reviewed

    A. Watanabe, N. Tamaki, K. Yokota, M. Matsuyama, S. Kokeguchi

    Journal of Hospital Infection   99 ( 3 )   303 - 305   2018.7

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    Aerosol and splatter produced during dental treatments (ultrasonic scaling and professional mechanical tooth cleaning) are potential sources of infection. Contamination patterns on the mask, goggles, chest and gowned right arm of operators, and on the goggles of patients before and after dental treatments were investigated using ATP bioluminescence analysis. Contamination on every surface tested increased significantly after dental treatment. Maximum contamination was found on the goggles of patients. Aerosol and splatter produced during dental treatments therefore have the potential to spread infection to operators and patients. ATP bioluminescence is a useful tool for monitoring surface contamination.

    DOI: 10.1016/j.jhin.2018.03.002

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  • Vibrio alginolyticus VepA Induces Lysosomal Membrane Permeability and Cathepsin-Independent Cell Death.

    Agus Eka Darwinata, Kazuyoshi Gotoh, Takehiko Mima, Yumiko Yamamoto, Kenji Yokota, Osamu Matsushita

    Acta medica Okayama   72 ( 3 )   231 - 239   2018.6

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    The bacterium Vibrio alginolyticus, an opportunistic pathogen in humans, has a type III secretion system (T3SS) that is responsible for its cytotoxicity toward eukaryotic cells. The effector of T3SS that is responsible for the cytotoxicity had not been identified. Here we demonstrate that VepA, a homolog of the T3SS effector in V. parahaemolyticus, is required for cytotoxicity in V. alginolyticus. VepA induces lysosomal membrane permeabilization, and it allows the leakage of only small molecules into the cytosol. Our findings revealed that VepA induces cathepsin-independent cell death in mammalian cells. The ferrous ion, one of the small molecules in the lysosome contents, appears to be involved in the cell death caused by V. alginolyticus VepA.

    DOI: 10.18926/AMO/56068

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  • DEC205 mediates local and systemic immune responses to Helicobacter pylori infection in humans. International journal

    Masahide Kita, Kenji Yokota, Chihiro Kageyama, Susumu Take, Kazuyoshi Goto, Yoshiro Kawahara, Osamu Matsushita, Hiroyuki Okada

    Oncotarget   9 ( 22 )   15828 - 15835   2018.3

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    Helicobacter pylori infections cause gastritis and affect systemic immune responses; however, no direct association between immune cells and stomach bacteria has yet been reported. The present study investigated DEC205-mediated phagocytosis of H. pylori and the role of DEC205-positive macrophages in the human gastric mucosa. DEC205 mediated phagocytosis of H. pylori was detected immunocytochemically in PMA-stimulated macrophages differentiated from NOMO1 cells. Expression of DEC205 mRNA in peripheral blood mononuclear cells (PBMCs) from H. pylori-infected patients was analyzed following stimulation with H. pylori cell lysate. We found that anti-DEC205 antibodies inhibited phagocytosis of H. pylori. The number of cells double-positive for DEC205 and CD14 in human gastric mucosa was higher in H. pylori-infected patients. DEC205-positive macrophages invaded the extracellular space between epithelial cells within gastric pits. In addition, DEC205 mRNA expression was upregulated in human PBMCs stimulated with H. pylori lysate. These findings suggest DEC205-expressing macrophages are important for recognition of H. pylori in human gastric mucosa, which affects systemic immunity.

    DOI: 10.18632/oncotarget.24574

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  • Low incidence of esophageal adenocarcinoma after eradication of Helicobacter pylori in Japan. Reviewed International journal

    Take S, Mizuno M, Ishiki K, Hamada F, Yoshida T, Yokota K, Okada H

    Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association   16 ( 12 )   1995 - 1996   2018.3

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    DOI: 10.1016/j.cgh.2018.03.030

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  • 細菌性コラゲナーゼのPKDドメインの構造機能解析と骨新生誘導剤の開発(Structure analysis of bacterial collagenases to develop therapeutics to induce osteogenesis) Reviewed

    松下 治, 内田 健太郎, 美間 健彦, 後藤 和義, 山本 由弥子, 横田 憲治, Bauer Ryan, 高相 晶士, Sakon Joshua

    日本細菌学雑誌   73 ( 1 )   114 - 114   2018.2

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  • Elevated serum interferon gamma-induced protein 10 kDa is associated with TAFRO syndrome Reviewed

    Noriko Iwaki, Yuka Gion, Eisei Kondo, Mitsuhiro Kawano, Taro Masunari, Hiroshi Moro, Koji Nikkuni, Kazue Takai, Masao Hagihara, Yuko Hashimoto, Kenji Yokota, Masataka Okamoto, Shinji Nakao, Tadashi Yoshino, Yasuharu Sato

    SCIENTIFIC REPORTS   7   42316   2017.2

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    Multicentric Castleman disease (MCD) is a heterogeneous lymphoproliferative disorder. It is characterized by inflammatory symptoms, and interleukin (IL)-6 contributes to the disease pathogenesis. Human herpesvirus 8 (HHV-8) often drives hypercytokinemia in MCD, although the etiology of HHV-8-negative MCD is idiopathic (iMCD). A distinct subtype of iMCD that shares a constellation of clinical features including thrombocytopenia (T), anasarca (A), fever (F), reticulin fibrosis (R), and organomegaly (O) has been reported as TAFRO-iMCD, however the differences in cytokine profiles between TAFRO-iMCD and iMCD have not been established. We retrospectively compared levels of serum interferon gamma-induced protein 10 kDa (IP-10), platelet-derived growth factor (PDGF)-AA, interleukin (IL)-10, and other cytokines between 11 cases of TAFRO-iMCD, 6 cases of plasma cell type iMCD, and 21 healthy controls. During flare-ups, patients with TAFRO-iMCD had significantly higher serum IP-10 and tended to have lower PDGF-AA levels than the other 2 groups. In addition, serum IL-10, IL-23, and vascular endothelial growth factor-A were elevated in both TAFRO-iMCD and iMCD. Elevated serum IP-10 is associated with inflammatory diseases including infectious diseases. There was a strong correlation between high serum IP-10 and the presence of TAFRO-iMCD, suggesting that IP-10 might be involved in the pathogenesis of TAFRO-iMCD.

    DOI: 10.1038/srep42316

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  • Monitoring of bacterial contamination of dental unit water lines using adenosine triphosphate bioluminescence. Reviewed International journal

    Watanabe A, Tamaki N, Yokota K, Matsuyama M, Kokeguchi S

    The Journal of hospital infection   94 ( 4 )   393 - 396   2016.12

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    Bacterial contamination of dental unit waterlines (DUWLs) was evaluated using ATP bioluminescence analysis and a conventional culture method. Water samples (N=44) from DUWLs were investigated for heterotrophic bacteria by culture on R2A agar, which gave counts ranging from 1.4×103 to 2.7×105 cfu/mL. The ATP bioluminescence results for DUWL samples ranged from 6 to 1189 relative light units and could be obtained within 1min; these correlated well with the culture results (r=0.727-0.855). We conclude that the results of the ATP bioluminescence assay accurately reflect the results of conventional culture-based testing. This method is potentially useful for rapid and simple monitoring of DUWL bacterial contamination.

    DOI: 10.1016/j.jhin.2016.08.001

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  • Geranylgeranylacetone selectively binds to the HSP70 of Helicobacter pylori and alters its coccoid morphology Reviewed

    Ewa Grave, Shin-ichi Yokota, Soh Yamamoto, Arisa Tamura, Takako Ohtaki-Mizoguchi, Kenji Yokota, Keiji Oguma, Kazuhiko Fujiwara, Nobuaki Ogawa, Tomoya Okamoto, Michiro Otaka, Hideaki Itoh

    SCIENTIFIC REPORTS   5   13738   2015.9

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    Geranylgeranylacetone (GGA) is used to treat patients suffering from peptic ulcers and gastritis. We examined the effect of GGA on Helicobacter pylori, which is a causative factor of gastrointestinal diseases. Previously, we have reported that GGA binds specifically to the molecular chaperone HSP70. In this paper, we report that GGA bounds to H. pylori HSP70 (product of the DnaK gene) with 26-times higher affinity than to human HSP70, and induced large conformational changes as observed from surface plasmon resonance and circular dichroism. Binding of GGA suppressed the activity of the H. pylori chaperone. GGA also altered several characteristics of H. pylori cells. GGA-treated cells elicited enhanced interleukin-8 production by gastric cancer cell lines and potentiated susceptibility to complement as compared to untreated cells. GGA also caused morphological alterations in H. pylori as reflected in fewer coccoid-like cells, suggesting that GGA converts H. pylori to an actively dividing, spiral state (vegetative form) from a non-growing, coccoid state. This morphological conversion by GGA resulted in accelerated growth of H. pylori. These results suggest a model in which GGA sensitizes H. pylori to antibiotic treatment by converting the cells to an actively growing state.

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  • 口腔清掃と洗口との併用効果の検討 口腔内細菌数を指標にして

    渡辺 朱理, 横田 憲治, 松山 美和, 苔口 進

    日本歯科衛生学会雑誌   10 ( 1 )   120 - 120   2015.8

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  • Seventeen-year effects of eradicating Helicobacter pylori on the prevention of gastric cancer in patients with peptic ulcer; a prospective cohort study Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Fumihiro Hamada, Tomowo Yoshida, Kenji Yokota, Hiroyuki Okada, Kazuhide Yamamoto

    JOURNAL OF GASTROENTEROLOGY   50 ( 6 )   638 - 644   2015.6

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    We previously reported that eradication of Helicobacter pylori in our cohort of patients with peptic ulcer disease reduced their risk of developing gastric cancer to approximately one-third after a mean follow-up period of 3.4 years (up to 8.6 years). We have now followed these patients for a longer period.
    A total of 1,222 consecutive patients with peptic ulcer diseases who completed more than 1-year follow-up after receiving H. pylori eradication therapy were followed with annual endoscopic surveillance for a mean of 9.9 years (as long as 17.4 years).
    H. pylori infection was judged cured in 1,030 patients (eradication-success group) but persisted in 192 (eradication-failure group) after initial eradication therapy. In the eradication-failure group, 114 patients received re-treatment at a mean of 4.4 years after the start of follow-up, and 105 of these were cured of infection. Gastric cancer developed in 21 of the 1,030 patients in the eradication-success group and in nine of the 192 in the failure group (p = 0.04). The risk of developing gastric cancer in the eradication-success group (0.21 %/year) was significantly lower than that in the failure group (0.45 %, p = 0.049). The longest interval between the initial H. pylori eradication and the occurrence of gastric cancer was 14.5 years in the eradication-success group and 13.7 years in the eradication-failure group.
    A prophylactic effect for gastric cancer persists for more than 10 years after H. pylori eradication therapy, but we should be aware that cancer can develop even after that interval.

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  • [A Study to Determine the Optimum Antigens for the Serodiagnosis of Helicobacter Pylori Infection in Japanese Patients and the Association with IgG Subclass and Gastric Cancer]. Reviewed

    Kita M, Take S, Okada H, Matsushita O, Yokota K

    Rinsho byori. The Japanese journal of clinical pathology   63 ( 2 )   180 - 186   2015.2

  • 細菌必須遺伝子を標的とする阻害リード化合物の口腔細菌に対する効果

    苔口 進, 狩山 玲子, 横田 憲治, 渡辺 朱理

    日本環境感染学会誌   30 ( Suppl. )   438 - 438   2015.1

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  • 環境汚染菌の消毒剤含浸ワイプによる拭き取り効果の検討

    横田 憲治, 渡邉 都貴子, 林 俊治, 渡辺 朱理, 苔口 進, 平井 義一

    日本環境感染学会誌   30 ( Suppl. )   206 - 206   2015.1

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  • Antibacterial activity of a novel synthetic progesterone species carrying a linoleic acid molecule against Helicobacter pylori and the hormonal effect of its steroid on a murine macrophage-like cell line Reviewed

    Avarzed Amgalanbaatar, Hirofumi Shimomura, Kouichi Hosoda, Shunji Hayashi, Kenji Yokota, Yoshikazu Hirai

    JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY   140   17 - 25   2014.3

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    Helicobacter pylori, a pathogen responsible for gastric and duodenal diseases, absorbs various steroid compounds into the cell membrane even though some are toxic to this bacterium. An earlier study by our group has demonstrated that progesterone is bactericidal to H. pylori. In this study, we newly synthesized a steroid compound, 17 alpha-hydroxyprogesterone linoleic acid ester (17hPL), to examine antibacterial activity against H. pylori. As expected, 17hPL acted as a bactericidal agent to H. pylori and had no effect on the survival of other common bacterial species. This steroidal substance interacted with phosphatidylethanolamine (PE) on the outer membrane of H. pylori to induce the release of PE from the bacterial cell membrane and to ultimately lyse the bacterial cells. One of the hormonal effects of progesterone is the inhibition of nitric oxide (NO) production from mouse macrophages activated by lipopolysaccharide (LPS). We therefore examined the inhibition effect of 17hPL on the NO production of RAW 264.7 cells, a murine macrophage-like cell line, stimulated with LPS and demonstrated that 17hPL is relatively weaker in its capability to inhibit NO production in LPS-activated cells than progesterone. These results suggest the possibility that 17hPL could be an oral medicine for selectively treating patients infected with H. pylori. (C) 2013 Elsevier Ltd. All rights reserved.

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  • 病院内の環境細菌調査

    横田 憲治, 渡邉 都貴子, 苔口 進, 林 俊治, 平井 義一

    日本環境感染学会誌   29 ( Suppl. )   287 - 287   2014.1

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  • [New Helicobacters other than H. pylori]. Reviewed

    Yokota K, Kita M, Okada H, Matsushita O, Oguma K

    Nihon rinsho. Japanese journal of clinical medicine   71 ( 8 )   1374 - 1379   2013.8

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    Since discovery of Helicobacter pylori, more than 30 species non-H. pylori Helicobacter spp. (NHPH) have been reported. Those NHPH were now classified into gastric Helicobacter spp. and enterohepatic Helicobacter spp.(EHS). Gastric NHPH show tight spiral and long shape in the gastric mucosa, and we can distinguish from H. pylori by light microscope. Some gastric NHPH may be zoonosis and cause gastritis in human. H. hepaticus and H. cinaedi belongs in EHS were detected in human diseases. H. hepaticus may be associated with hepatobiliary diseases in humans. Surprisingly, it was reported that H. cinaedi infection was associated with atrial arrhythmias and atherosclerosis. Many NHPH will be recognized as human pathogen in the future.

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  • The Genetic Diversity of Helicobacter pylori Virulence Genes Is Not Associated with Gastric Atrophy Progression Reviewed

    Masahide Kita, Kenji Yokota, Hiroyuki Okada, Susumu Take, Ryuta Takenaka, Yoshiro Kawahara, Keiji Oguma, Osamu Matsushita, Kazuhide Yamamoto

    ACTA MEDICA OKAYAMA   67 ( 2 )   93 - 98   2013.4

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    Atrophy of the gastric mucosa is a precursor of intestinal-type gastric cancer, and Helicobacter pylori infection causes atrophic gastritis. The aim of this study was to determine whether the genetic diversity of H. pylori virulence genes is associated with the development and progression of gastric atrophy in humans. We isolated and cultured H. pylori strains from patients with gastric ulcer and duodenal ulcer accompanied by atrophic gastritis in background mucosa. H. pylori strains were stored at -80 degrees C prior to the experiments being carried out. We analyzed iceA, babA, vacA, cagA, and cagE genes by PCR. The cagA gene was analyzed through sequencing of the C-terminal region containing the EPIYA motif, which is related to tyrosine phosphorylation. Severe atrophy was observed in patients with gastric ulcer. The major phenotype of the vacA gene was slc/ml (93%). The cagA gene was detected in all strains. The cagE gene was not detected in 2 and 5 strains from the mild cases and severe cases, respectively. The major cagA EPIYA motif, which is amino acids repeat in the C terminus, was the A-B-D type (44 of 58 strains). The virulence genes were not statistically associated with the severity of atrophy in the background gastric mucosa in humans. Not only identification of bacterial virulence factors but also studies of the host response will be necessary to investigate the progression of gastric atrophy and subsequent cancer development in humans.

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  • Detoxification of 7-Dehydrocholesterol Fatal to Helicobacter pylori Is a Novel Role of Cholesterol Glucosylation Reviewed

    Hirofumi Shimomura, Kouichi Hosoda, David J. Mcgee, Shunji Hayashi, Kenji Yokota, Yoshikazu Hirai

    JOURNAL OF BACTERIOLOGY   195 ( 2 )   359 - 367   2013.1

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    The glucosylation of free cholesterol (FC) by Helicobacter pylori cells has various biological significances for the survival of this bacterium. H. pylori cells with glucosylated FC are capable of evading host immune systems, such as phagocytosis by macrophages and activation of antigen-specific T cells, and surviving in the gastric mucosal tissues for long periods. An additional role of cholesterol glucosylation in the survival of H. pylori which is distinct from the role of escaping the host immune system, however, has yet to be identified. This study demonstrated that 7-dehydrocholesterol (7dFC), an FC precursor, is a toxic compound fatal to H. pylori cells, but the cell membrane of H. pylori is capable of absorbing this toxic sterol via glucosylation. In contrast to the case with 7dFC, no toxicity to H. pylori cells was detected from the glucosylated 7dFC. In addition, cgt gene mutant H. pylori cells that cannot glucosylate cholesterols had higher susceptibility to the toxic action of 7dFC than wild-type H. pylori cells. These results indicate that the cgt gene product of H. pylori serves to detoxify the sterol fatal to this bacterium and to permit this toxic sterol as a cell membrane lipid component. In summary, this study defined a novel role of cholesterol glucosylation in H. pylori.

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  • Reinfection rate of Helicobacter pylori after eradication treatment: a long-term prospective study in Japan Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Takayuki Imada, Tetsuji Okuno, Tomowo Yoshida, Kenji Yokota, Keiji Oguma, Masahide Kita, Hiroyuki Okada, Kazuhide Yamamoto

    JOURNAL OF GASTROENTEROLOGY   47 ( 6 )   641 - 646   2012.6

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    We previously reported that the reinfection rate with Helicobacter pylori in Japan was low despite a high prevalence of infection. In the present study, we extended our previous work to more accurately determine the reinfection rate.
    We enrolled 1625 patients (219 women and 1406 men, mean age 50.8 years) who had received H. pylori eradication therapy. After documentation of eradication, bacterial culture and urea breath test were carried out yearly. H. pylori strains were analyzed by using random amplification of polymorphic DNA fingerprinting.
    A total of 1609 patients were followed for up to 12.5 years (mean 4.7 years); H. pylori became re-positive in 26 patients. In 13 of the 26 patients, H. pylori became positive at the first-year follow up. Stored H. pylori isolates were available for analysis from ten of the 13 patients; four of the isolates were genetically different from the initial strain, but the other six were identical to the initial strain. In the other 13 patients, H. pylori became positive at later follow up (mean 4.8 years; range 1.8-8.0 years). In all of the four of these patients whose isolates could be analyzed, the H. pylori strains were different from the initial strain. Assuming that reinfection occurred in the four patients positive for different strains of H. pylori at the first-year follow up and in the 13 positive at later follow up, the reinfection rate was 0.22% per year.
    When probable recrudescence (H. pylori positivity with identical strains) was excluded, the reinfection rate of H. pylori in this Japanese population was very low, but we note that reinfection can occur over many years.

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  • Clostridium botulinum Type E Toxins Bind to Caco-2 Cells by a Different Mechanism from That of Type A Toxins Reviewed

    Kai Zhang, Yumiko Yamamoto, Tomonori Suzuki, Kenji Yokota, Shaobo Ma, Ni Nengah Dwi Fatmawati, Keiji Oguma

    ACTA MEDICA OKAYAMA   66 ( 3 )   253 - 261   2012.6

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    Cultured Clostridium botulinum strains produce progenitor toxins designated as 12S, 16S, and 19S toxins. The 12S toxin consists of a neurotoxin (NTX, 7S) and a non-toxic non-hemagglutinin (NTNH). The 16S and 19S toxins are formed by conjugation of the 12S toxin with hemagglutinin (HA), and the 19S toxin is a dimer of the 16S toxin. Type A cultures produce all 3 of these progenitor toxins, while type E produces only the 12S toxin. The 7S toxin is cleaved into heavy (H) and light (L) chains by a protease(s) in some strains, and the H chain has 2 domains, the N-terminus (Hn) and C-terminus (Hc). It has been reported that type A toxins bind to the intestinal cells or cultured cells via either HA or Hc. In this study, we investigated the binding of type A and E toxins to Caco-2 cells using Western blot analysis. Both the type E 7S and 12S toxins bound to the cells, with the 7S toxin binding more strongly, whereas, in the type A strain, only the 16S/19S toxins showed obvious binding. Pre-incubation of the type E 7S toxin with IgG against recombinant type E Hc significantly inhibited the 7S toxin binding, indicating that He might be a main binding domain of the type E toxin.

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  • Phosphatidylethanolamine of Helicobacter pylori Functions as a Steroid-Binding Lipid in the Assimilation of Free Cholesterol and 3 beta-Hydroxl Steroids into the Bacterial Cell Membrane Reviewed

    Hirofumi Shimomura, Kouichi Hosoda, Shunji Hayashi, Kenji Yokota, Yoshikazu Hirai

    JOURNAL OF BACTERIOLOGY   194 ( 10 )   2658 - 2667   2012.5

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    One of the unique features of Helicobacter pylori is its ability to assimilate free-cholesterol (FC) into its membranes. Via FC assimilation, H. pylori strengthens the membrane lipid barrier and/or evades the host immune system. No previous studies, however, have investigated the FC uptake mechanisms of the H. pylori cell. Phosphatidylethanolamine (PE) is the most prevalent lipid component of bacteria, including H. pylori, but the function of PE remains unclear. We were therefore interested in H. pylori PE (HpPE) and investigated the interaction of its PE with cholesterols. The PE isolated from H. pylori underwent a unique molecular interaction with FC, cholesterol ester (CE), and 2,6-di-O-methyl-beta-cyclodextrin (dM beta CD), a sterol solubilizer. HpPE interacted not only with the FC molecule, but also with the FC-dM beta CD inclusion complex. In contrast, Escherichia coli PE (EcPE), prepared as a reference PE, seemed to bind only FC, and only via a hydrophobic interaction, without binding dM beta CD. HpPE was clearly more potent than EcPE in binding FC. Intriguingly, HpPE had a negligible affinity for CE, while EcPE had a high affinity for CE, comparable to its affinity for FC. Further, HpPE interacted with 3 beta-OH steroids, pregnenolone and dehydroepiandrosterone, in the absence of dM beta CD. Gas chromatogram-mass spectrometry (GC-MS) and liquid chromatography-mass spectrometry (LC-MS) analyses revealed that the fatty acid compositions of HpPE were quite distinct from those of EcPE, and the C-14:0 fatty acid in the HpPE molecule was found to be significant in binding FC selectively. These results indicate that PE is a key candidate of nonesterified steroid-binding lipids in H. pylori.

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  • Role of heat shock protein derived from Streptococcus sanguinis in Behcet’s disease Reviewed

    Kaneko F, Togashi A, Nomura E, Isogai E, Yokota K, Oguma K

    J Med Micorobiol Diagnosis   2012

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  • Steroid hormones as bactericidal agents to Helicobacter pylori Reviewed

    Kouichi Hosoda, Hirofumi Shimomura, Shunji Hayashi, Kenji Yokota, Yoshikazu Hirai

    FEMS MICROBIOLOGY LETTERS   318 ( 1 )   68 - 75   2011.5

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    Helicobacter pylori is a unique bacterial species that assimilates various steroids as membrane lipid components. Our group has recently found, however, that certain steroids may impair the viability of H. pylori. In this study, we go on to reveal that estradiol, androstenedione, and progesterone (PS) all have the potential to inhibit the growth of H. pylori. Of these three steroid hormones, progesterone demonstrated the most effective anti-H. pylori action. 17 alpha-hydroxyprogesterone caproate (17 alpha PSCE), a synthetic progesterone derivative, had a much stronger anti-H. pylori action than progesterone, whereas 17 alpha-hydroxyprogesterone, a natural progesterone derivative, completely failed to inhibit the growth of the organism. Progesterone and 17 alpha PSCE were both found to kill H. pylori through their bacteriolytic action. Among five bacterial species investigated, H. pylori was the only species susceptible to the bactericidal action of progesterone and 17 alpha PSCE. The other four species, Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, and Staphylococcus epiderimidis, all resisted this action. Progesterone and free-cholesterol (FC) obstructed each other's effects against the H. pylori cell. Taken in sum, these results suggest that progesterone and FC may bind to the identical region on the H. pylori cell surface. We expect these findings to contribute to the development of a novel anti-H. pylori steroidal agent.

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  • The long-term risk of gastric cancer after the successful eradication of Helicobacter pylori Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Tomowo Yoshida, Nobuya Ohara, Kenji Yokota, Keiji Oguma, Hiroyuki Okada, Kazuhide Yamamoto

    JOURNAL OF GASTROENTEROLOGY   46 ( 3 )   318 - 324   2011.3

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    We previously reported that eradication of Helicobacter pylori reduced the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up our patient group to investigate the occurrence and clinical features of gastric cancers that developed after cure of the infection.
    Prospective post-eradication evaluations were conducted on 1674 consecutive patients who had received successful H. pylori eradication therapy. The patients had undergone endoscopic examination before eradication therapy to evaluate peptic ulcers, background gastric mucosal atrophy, and H. pylori infection. After confirmation of cure of the infection, follow-up endoscopy was performed yearly.
    The patients were followed for up to 14.1 years (a mean of 5.6 years). During the follow-up, gastric cancer developed in 28 of the 1674 patients as long as 13.7 years after the cure of H. pylori infection. The risk of developing gastric cancer was 0.30% per year. Histologically, 16 of the gastric cancers were the intestinal type and 12 were the diffuse type; the risk of each cancer type was 0.17 and 0.13% per year, respectively. There was no significant inflammatory cell infiltration in the background gastric mucosa at the time the cancers were recognized.
    There is a risk of developing gastric cancer of both the intestinal and diffuse types even after the cure of H. pylori infection and extinction of gastric inflammation. It is important to inform patients about the risk of gastric cancer after eradication therapy and offer them surveillance endoscopy.

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  • Behcet's Disease (Adamantiades-Behcet's Disease) Reviewed

    Fumio Kaneko, Ari Togashi, Sanae Saito, Hideo Sakuma, Noritaka Oyama, Koichiro Nakamura, Kenji Yokota, Keiji Oguma

    CLINICAL & DEVELOPMENTAL IMMUNOLOGY   2011   681956   2011

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    Adamantiades-Behcet's disease (ABD) is characterized by starting with oral aphthous ulceration and developing of the systemic involvements. The pathogenesis of ABD is closely correlated with the genetic factors and the triggering factors which acquire delayed-type hypersensitivity reaction against oral streptococci mediated by IL-12 cytokine family. HLA-B51 is associated in more than 60% of the patients and its restricted CD8+ T cell response is clearly correlated with the target tissues. Bes-1 gene encoded partial S. sanguinis genome which is highly homologous with retinal protein, and 65 kD heat shock protein (Hsp-65) released from streptococci is playing an important role with human Hsp-60 in the pathogenesis of ABD. Although Hsp-65/60 has homologies with the respective T cell epitope, it stimulates peripheral blood mononuclear cells (PBMCs) from ABD patients. On the other hand, some peptides of Hsp-65 were found to reduce IL-8 and IL-12 production from PBMCs of ABD patients in active stage.

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  • Passive Oral Immunization by Egg Yolk Immunoglobulin (IgY) to Vibrio cholerae Effectively Prevents Cholera Reviewed

    Kazuyuki Hirai, Hideyuki Arimitsu, Koji Umeda, Kenji Yokota, Lianhua Shen, Kiyoshi Ayada, Yoshikatsu Kodama, Takao Tsuji, Yoshikazu Hirai, Keiji Oguma

    ACTA MEDICA OKAYAMA   64 ( 3 )   163 - 170   2010.6

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    In an attempt to prepare egg yolk immunoglobulin (IgY) to treat and prevent cholera, hens were immunized by a mixture of heat- or formalin-killed Vibrio cholerae O1 and O139 organisms, or by the recombinant cholera toxin B subunit (CTB). The IgYs were partially purified from egg yolk and orally administered to suckling mice before or after challenge with live O1 or O139 cells. The anti-O1 and O139 IgYs and the mixture of either IgY with anti-CTB IgY significantly protected the occurrence of cholera caused by both O1 and O139 infection. Since large amounts of IgY can be prepared very easily and at low cost, this seems to be a useful procedure for preventing and treating cholera.

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  • コレラ菌およびコレラ毒素Bサブユニットに対するニワトリ抗体(IgY)の有用性

    平井 一行, 衛藤 友美, 大野 佑子, 田村 臣哉, 山本 由弥子, 難波 ひかる, 阪口 義彦, 横田 憲治, 小熊 惠二

    日本薬学会年会要旨集   130年会 ( 3 )   84 - 84   2010.3

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  • Steroids mediate resistance to the bactericidal effect of phosphatidylcholines against Helicobacter pylori Reviewed

    Hirofumi Shimomura, Kouichi Hosoda, Shunji Hayashi, Kenji Yokota, Keiji Oguma, Yoshikazu Hirai

    FEMS MICROBIOLOGY LETTERS   301 ( 1 )   84 - 94   2009.12

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    Helicobacter pylori assimilates various steroids as membrane lipid components, but it can also survive in the absence of steroids. It thus remains to be clarified as to why the organism relies on steroid physiologically. In this study, we have found that phosphatidylcholine carrying a linoleic acid molecule or arachidonic acid molecule has the potential to kill steroid-free H. pylori. The bactericidal action of phosphatidylcholines against H. pylori was due to the lytic activity of the phosphatidylcholines themselves and not due to the lytic activity of the unsaturated fatty acids or lyso-phosphatidylcholine resulting from the hydrolysis of the phosphatidylcholines. In contrast to the steroid-free H. pylori, the organism that absorbed and glucosylated free cholesterol was unaffected by the bactericidal action of the phosphatidylcholines. Similarly, H. pylori that absorbed estrone without glucosylating it also resisted the bactericidal action of the phosphatidylcholines. The steroids absorbed by H. pylori existed in both the outer and inner membranes, while the glucosyl-steroids produced via the steroid absorption were localized in the outer membrane rather than in the inner membrane. These results indicate that H. pylori absorbs the steroids to reinforce the membrane lipid barrier and thereby expresses resistance to the bacteriolytic action of hydrophobic compounds such as phosphatidylcholine.

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  • Detection of Helicobacter hepaticus in Human Bile Samples of Patients with Biliary Disease Reviewed

    Toshihide Hamada, Kenji Yokota, Kiyoshi Ayada, Kazuyuki Hirai, Tomoari Kamada, Ken Haruma, Kazuaki Chayama, Keiji Oguma

    HELICOBACTER   14 ( 6 )   545 - 551   2009.12

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    Background: Since the discovery of Helicobacter pylori, various enterohepatic Helicobacter spices have been detected in the guts of humans and animals. Some enterohepatic Helicobacters have been associated with inflammatory bowel disease or liver disease in mice. However the association of these bacteria with human diseases remains unknown. Materials and
    Methods: We collected 126 bile samples from patients with cholelithiasis, cholecystitis, gallbladder polyp, and other nonbiliary diseases. Samples were screened for the presence of enterohepatic Helicobacter spp. using Cultures, nested PCR, or in situ hybridization. We tested for antibodies to H. pylori and H. hepaticus by Western blot analysis.
    Results: Attempts at cultivation were unsuccessful. However, H. hepaticus was detected in bile samples with nested PCR whereas H. bilis was not. Helicobacter hepaticus in the bile was confirmed by in situ hybridization, but H. hepaticus from bile samples was coccoid in appearance. We detected immunoglobulin G antibodies to H. hepaticus in bile samples by Western blotting. Helicobacter hepaticus was detected in 40 (32%) of total 126 samples as H. hepaticus positive if at least one of the three methods with nested PCR, in situ, or Western blotting. Patients with cholelithiasis (41%) and cholecystitis with gastric cancer (36%) had significantly higher (p = .029) prevalence of H. hepaticus infection than samples from patients with other diseases.
    Conclusion: Helicobacter hepaticus may closely associate with diseases of the liver and biliary tract in humans.

    DOI: 10.1111/j.1523-5378.2009.00729.x

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  • Anabolic utilization of steroid hormones in Helicobacter pylori Reviewed

    Kouichi Hosoda, Hirofumi Shimomura, Shunji Hayashi, Kenji Yokota, Keiji Oguma, Yoshikazu Hirai

    FEMS MICROBIOLOGY LETTERS   297 ( 2 )   173 - 179   2009.8

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    In this study, we have demonstrated that Helicobacter pylori absorbs a steroid prehormone (pregnenolone) and two androgens (dehydroepiandrosterone and epiandrosterone), glucosylates these steroids, and utilizes glucosyl-steroid hormone compounds as the membrane lipid components. The only common structure among the steroid prehormone and the two androgens is a 3 beta-OH in the steroid framework. Our results indicate that the 3 beta-OH in the steroid hormones is a crucial conformation required for steroid glucosylation by H. pylori. In addition, we found that H. pylori absorbs and holds estrogens possessing 3-OH (estrone and estradiol) into the membrane. The effective absorption of estrogen into the membrane appeared to be controlled by the number of hydroxyl groups modifying the steroid framework. In contrast, H. pylori induced neither membrane absorption nor glucosylation of the other steroid hormones possessing 3=O (progesterone, androstenedione and testosterone) or 3 alpha-OH (androsterone). These results indicate that H. pylori selectively absorbs 3 beta-OH and 3-OH steroid hormones, and utilizes only 3 beta-OH steroid hormones as the materials for glucosylation.

    DOI: 10.1111/j.1574-6968.2009.01685.x

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  • Helicobacter pylori eradication may induce de novo, but transient and mild, reflux esophagitis: Prospective endoscopic evaluation Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Kenji Yokota, Keij Oguma, Hiroyuki Okada, Kazuhide Yamamoto

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   24 ( 1 )   107 - 113   2009.1

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    Backgrounds and Aim: The effect on reflux esophagitis of eradicating Helicobacter pylori is variable and not fully defined. We previously reported that in patients who have reflux esophagitis associated with duodenal ulcer, a significant improvement in the preexisting reflux esophagitis occurred after H. pylori was eradicated. In the present study, we asked whether H. pylori eradication leads to de novo development of reflux esophagitis in peptic ulcer patients.
    Methods: Prospective post-eradication evaluations were conducted in 1195 H. pylori-positive patients with peptic ulcer diseases who were confirmed not to have reflux esophagitis by endoscopic examination before eradication therapy. After eradication therapy, endoscopy and a urea breath test were performed yearly.
    Results: A total of 1187 patients were followed for up to 10.0 years (a mean of 3.6 years). Reflux esophagitis developed in 279 of 1000 patients cured of infection and in 26 of 187 patients who had persistent infection (P < 0.0001, Fisher's exact test). The esophagitis was mild (Los Angeles grade A) in most patients, transient in approximately one-half, and rarely necessitated long-term medication for the condition. Cure of infection, alcohol consumption, younger age, and high body mass index were identified as significant factors for the risk of developing non-transient reflux esophagitis.
    Conclusions: Cure of H. pylori infection may increase the risk of developing reflux esophagitis in patients with peptic ulcer, but the esophagitis is mostly mild and transient, and long-term medication is rarely required. Thus, H. pylori eradication therapy need not be withheld for fear of provoking reflux esophagitis.

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  • Helicobacter pylori heat shock protein 60 antibodies are associated with gastric cancer Reviewed

    Aki Tanaka, Tomoari Kamada, Kenji Yokota, Akiko Shiotani, Jiro Hata, Keiji Oguma, Ken Haruma

    PATHOLOGY RESEARCH AND PRACTICE   205 ( 10 )   690 - 694   2009

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    Helicobacter pylori infection causes atrophic gastritis, peptic ulcer, and gastric cancer. The host immune response plays an important role in the pathogenesis of H. pylori-related diseases. Heat shock proteins are antigens involved in various diseases This study evaluated seropositivity for antibodies to H. pylori heat shock protein 60 in patients with gastric cancer.
    Serum samples were obtained from 57 patients with gastric cancer (25 patients with diffuse-type gastric cancer and 32 with intestinal-type gastric cancer), 45 H. pylori-positive patients, and 49 H. pylori-negative patients without gastric cancer. Antibodies to heat shock protein 60 and H. pylori were assessed by enzyme-linked immunosorbent assay.
    The positivity rate for antibodies to hsp60 was significantly higher in H pylori-positive patients than in H. pylori-negative patients (73.3% vs. 24.5%. p<0.001). In addition, the positivity rate for antibodies to hsp60 was higher in patients with gastric cancer than in H. pylori-positive patients without gastric cancer (87.7% vs. 73.3%, p = 0.06), and the positivity rate for antibodies to hsp60 was significantly higher in patients with diffuse-type gastric cancer than in M pylori-positive patients Without gastric cancer (96% vs. 73 3%, p<0.05).
    H. pylori hsp60 might be associated with gastric carcinogenesis, especially in the case of diffuse cancer. (C) 2009 Elsevier GmbH. All rights reserved.

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  • Immune Reactions Against Elongation Factor 2 Kinase: Specific Pathogenesis of Gastric Ulcer from Helicobacter pylori Infection Reviewed

    Kiyoshi Ayada, Kenji Yokota, Yoshiro Kawahara, Yumiko Yamamoto, Kazuyuki Hirai, Tomoki Inaba, Masahide Kita, Hiroyuki Okada, Kazuhide Yamamoto, Keiji Oguma

    CLINICAL & DEVELOPMENTAL IMMUNOLOGY   2009

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    Helicobacter pylori (H. pylori) infection is a definite causative factor for gastric ulcers (GUs). In the present study we detected a specific antigen of gastric epithelial cells (HGC-27) using cell ELISA, which was recognized by the sera of GU patients (n = 20) but not in patients with chronic gastritis (CG; n = 20) or in healthy volunteers (HC; n = 10). This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting. The GU patients' lymphocytes stimulated by H. pylori specifically disrupted heat-stressed HGC-27 cells in a cytotoxic assay. In flow cytometry, the effector cells (lymphocytes) from GU patients were significantly differentiated to T helper type 1 lymphocyte (Th1) and cytotoxic T lymphocyte (CTL) as opposed to those from CG patients. The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress. This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU. Copyright (C) 2009 Kiyoshi Ayada et al.

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  • The role of streptococcal hypersensitivity in the pathogenesis of Behcet's Disease Reviewed

    Fumio Kaneko, Noritaka Oyama, Hirokatsu Yanagihori, Emiko Isogai, Kenji Yokota, Keiji Oguma

    EUROPEAN JOURNAL OF DERMATOLOGY   18 ( 5 )   489 - 498   2008.9

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    Behcet's disease (BID) is still considered as a mysterious multisysternic disorder characterized by recurrent involvement of muco-cutaneous, ocular, intestinal, vascular and/or nervous system organs. In this review, we would like to highlight and discuss several important advances in our understanding of the pathogenesis of BD based on the intrinsic genetic factors including HLA-B51 and MICA expression and extrinsic triggering factors. As one of the extrinsic triggering factors, we focused on the hypersensitivity against oral streptococci which might be acquired through the innate immune mechanism. It was found that HLA-B51 restricted CD8 T cell response was clearly correlated with the target tissues expressing MICA*009 by stress in active BD patients with HLA-B51 as the intrinsic factors. Bes-l gene and HSP-65 derived from oral S. sanguinis, which is the uncommon serotype (KTH-1, strain BDl13-20), are supposed to play important roles as an extrinsic factor in BD pathogenesis. The peptides of the Bes-l gene are highly homologous with the retinal protein Brn3b and moreover, the Bes-l peptides were homologous with HSP-65 derived from microorganisms in association with the counterpart human HSP-60, which appeared reactively in the patients. HSP-65/60 also has high homologies with the respective T cell epitope of BD patients. Although HSP-65/60 and the peptides of Bes-l gene were found to stimulate PBMCs from BD patients in the production of pro-inflammatory Th1 type cytokines, some homologous peptides of HSP-65 with T cell epitopes were found to reduce IL-8, IL-12 and TNF-alpha produced from PBMCs of active BID patients. The findings might be correlated with the clinically therapeutic effects for BD patients with severe uveitis, who were led to immunotolerance by the peptide of human HSP-60 (336-351), as previously reported. Then, the pathogenesis of BD was discussed referring to intrinsic genetic factors and extrinsic triggering factors in aspects of streptococcal hypersensitivity, which might be acquired through the innate immune mechanisms. The BD symptoms were thought to be due to vascular reactions as immune responses in correlation with monocyte expressed streptococcal agents.

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  • Antibodies against heat shock protein 60 derived from Helicobacter pylori: Diagnostic implications in cardiovascular disease

    Tomoyuki Okada, Kiyoshi Ayada, Shinichi Usui, Kenji Yokota, Jinhua Cui, Yoshiro Kawahara, Tomoki Inaba, Satoshi Hirohata, Motowo Mizuno, Daisuke Yamamoto, Shozo Kusachi, Eiji Matsuura, Keiji Oguma

    Journal of Autoimmunity   29 ( 2-3 )   106 - 115   2007.9

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    Immune responses against heat shock protein 60 (HSP60) of pathogen-origin are thought to be defensive events which, due to molecular mimicry, misdirect to a human counterpart. Therefore, atherosclerosis may be serologically predicted by anti-HSP60 antibodies (Abs). In the present study, we analyzed the clinical prevalence of the serum IgG Abs against Helicobacter pylori (Hp)-derived HSP60 (Hp-HSP60) or its peptide fragments in patients with cardiovascular disease (CVD; n = 250), as compared to those in age- and gender-matched non-CVD patients (n = 293). Anti-Hp cell lysate Abs frequently appeared in Hp-infected patients who were not associated with CVD. In contrast, Abs against the particular amino acid sequence Hp-HSP60II3 (II3 region, Glu141-Leu160, in Hp-HSP60) predominantly appeared in CVD patients, as well as IgG anti-human HSP60 (Hu-HSP60w). Furthermore, neither titer of anti-Hp-HSP60II3 nor anti-Hu-HSP60w Abs was correlated with the levels of high sensitivity C-reactive protein (hsCRP). This data strongly suggested that IgG anti-Hp-HSP60II3 Abs cross-reacted with Hu-HSP60w were independent diagnostic markers relevant to CVD. Further, the 20 amino acid residues (Glu141-Leu160) might be predominant CVD-associated epitopes that induce anti-Hu-HSP60 auto-Abs, whose location was predicted in the tertiary structure of Hu-HSP60. © 2007 Elsevier Ltd. All rights reserved.

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  • Conversion of flavodoxin from holoenzyme to apoprotein during growth phase changes in Helicobacter pylori Reviewed

    Hirofumi Shimomura, Shunji Hayashi, Kenji Yokota, Keiji Oguma, Yoshikazu Hirai

    JOURNAL OF BACTERIOLOGY   189 ( 13 )   4960 - 4963   2007.7

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    The catabolic pathway for flavodoxin has yet to be clarified for any bacterial species. In this study, we found that the flavin mononucleotide in the flavodoxin of Helicobacter pylori is degraded to riboflavin via the phosphomonoesterase activity of class C acid phosphatase. The result is a conversion of holoflavodoxin to apoflavodoxin.

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  • Helicobacter pylori heat-shock protein 60 induces interleukin-8 via a Toll-like receptor (TLR)2 and mitogen-activated protein (MAP) kinase pathway in human monocytes Reviewed

    Ying Zhao, Kenji Yokota, Kiyoshi Ayada, Yumiko Yamamoto, Tomayuki Okada, Lianhua Shen, Keiji Oguma

    JOURNAL OF MEDICAL MICROBIOLOGY   56 ( 2 )   154 - 164   2007.2

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    Previous reports have indicated that Helicobacter pylori heat-shock protein 60 (H. pylori-HSP60), as an immunodominant antigen, induces interleukin (IL)-8 production in human monocytes. The exact mechanism by which H. pylori-HSP60 induces IL-8 production in monocytes has not been fully elucidated. In the present study, the downstream pathway by which H. pylori-HSP60 induces IL-8 secretion in human monocytic cell lines was investigated. Intact H. pylori, heat-killed H. pylori and H. pylori recombinant HSP60 (rHpHSP60) all induced the secretion of IL-8 and the activation of mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) and p38, but not c-Jun N-terminal kinase (JNK), up to 24 In in NOMO1 cells. The specific inhibitors PD98059 and U0126 (for ERK1/2 signalling) and SB203580 (for p38 MAPK signalling) down-regulated IL-8 secretion from rHpHSP60-treated NOMO1 cells. An anti-Toll-like receptor (TLR)2 antibody or TLR2 small interfering RNA (siRNA) partialiy inhibited the secretion of IL-8, and anti-TLR2 antibody also suppressed activation of ERK and p38 MAPK in rHpHSP60-treated NOMO1 cells. These reactions were associated with nuclear factor-kappa B (NF-kappa B)-mediated transcriptional activation, since U01 26, SB203580 and the anti-TLR2 antibody decreased NF-kappa B activation. Taken together, the results suggest that ERK and p38 MAPK signalling linked to the TLR2 recognition receptor in human monocytes may be an important pathway in H. pylori-HSP60-induced IL-8 secretion.

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  • Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Kenji Yokota, Keiji Oguma

    JOURNAL OF GASTROENTEROLOGY   42   21 - 27   2007.1

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    Background. We previously reported that eradication of Helicobacter pylori could reduce the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up out-patient groups to identify factors associated with the development of gastric cancer. Methods. Prospective posteradication evaluations were conducted in 1342 consecutive patients (1191 men and 151 women; mean age, 50 years) with peptic ulcer disease who had received H. pylori eradication therapy. The patients had undergone endoscopic examination before eradication therapy to evaluate peptic ulcers, background gastric mucosa, and H. pylori infection. After confirmation of eradication, follow-up endoscopy was performed yearly. Results. A total of 1131 patients were followed for up to 9.5 years (mean, 3.9 years). Gastric cancer developed in 9 of 953 patients cured of infection and in 4 of 178 who had persistent infection (P = 0.04). The risk of developing gastric cancer after receiving H. pylori eradication therapy was increased according to the grade of baseline gastric mucosal atrophy (P = 0.01). In patients with peptic ulcer diseases, persistent infection of H. pylori (hazard ratio, 3.9; P = 0.03), the grade of baseline gastric mucosal atrophy (3.3, P = 0.01) and age (2.0, P = 0.04) were identified as significant risk factors for developing gastric cancer. Conclusions. The grade of gastric atrophy was closely related to the development of gastric cancer after receiving H. pylori eradication therapy. Thus, eradication of H. pylori before the significant expansion of atrophy is most beneficial to prevent gastric cancer.

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  • A better cure rate with 800 mg than with 400 mg clarithromycin regimens in one-week triple therapy for Helicobacter pylori infection in cigarette-smoking peptic ulcer patients Reviewed

    Hidehiko Ishioka, Motowo Mizuno, Susumu Take, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Hiroyuki Okada, Kenji Yokota, Keiji Oguma

    DIGESTION   75 ( 2-3 )   63 - 68   2007

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    Background/Aims: In Helicobacter pylori eradication therapy, using a proton pump inhibitor plus amoxicillin and clarithromycin (PPI/AC regimen), the impact of the clarithromycin dose and smoking on efficacy is conflicting. Here, we compared the efficacy of 400 and 800 mg of clarithromycin in the regimen in relation to smoking in patients with peptic ulcer disease. Methods: We studied 601H. pylori-positive patients with peptic ulcer disease who had received amoxicillin 750 mg and clarithromycin 200 or 400 mg together with lansoprazole 30 mg b. i. d. Results: 305 patients were treated with a regimen containing 400 mg of clarithromycin (C400 group), and 296 patients with a regimen containing 800 mg (C800 group). Overall cure rates between the two groups were not significantly different, but the cure rate in the C800 group was significantly better than that in the C400 group among patients infected with clarithromycin- sensitive strains (p = 0.03). This difference could be attributed to differences among smokers versus non-smokers: the cure rate among smokers in the C800 group (91.0%) was better than that in the C400 group (80.0%, p = 0.003). Conclusions: 800 mg of clarithromycin is recommended in the PPI/AC regimen for patients who smoke and are infected with clarithromycinsensitive H. pylori.

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  • Production of anti-neurotoxin antibody is enhanced by two subcomponents, HA1 and HA3b, of Clostridium botulinum type B 16S toxin–haemagglutinin Reviewed

    Jae-Chul Lee, Kenji Yokota, Hideyuki Arimitsu, Hyun-Jung Hwang, Yoshihiko Sakaguchi, Jinhua Cui, Kouichi Takeshi, Toshihiro Watanabe, Tohru Ohyama, Keiji Oguma

    Microbiology   151 ( 11 )   3739 - 3747   2005.11

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    <italic>Clostridium botulinum</italic> type B strain produces two forms of progenitor toxin, 16S and 12S. The 12S toxin is formed by association of a neurotoxin (NTX) and a non-toxic non-haemagglutinin (NTNH), and the 16S toxin is formed by conjugation of the 12S toxin with a haemagglutinin (HA). HA consists of four subcomponents designated HA1, HA2, HA3a and HA3b. When mice were immunized with formalin-detoxified NTX, 12S or 16S, a significantly greater amount of anti-NTX antibody (Ab) was produced in the mice injected with 16S than in NTX- or 12S-injected mice. Immunization with NTX mixed with HA1 and/or HA3b also increased the anti-NTX Ab production, whereas NTX mixed with HA2 did not, indicating that HA1 and HA3b have adjuvant activity. This was further confirmed by immunizing mice with human albumin (Alb) alone or Alb mixed with either HA1 or HA3b. When mouse-spleen cells were stimulated with NTX, 16S or different HA subcomponents, 16S, HA1, HA3b and the mixture of HA1 and HA3 significantly increased interleukin 6 (IL6) production compared with NTX alone. Transcription of IL6 mRNA was low after stimulation with NTX alone, but increased to 16S-stimulation levels when NTX was mixed with HA1 or HA3b. In flow cytometry using labelled Abs against CD3 and CD19, the percentage of CD19 cells was higher following stimulation with 16S or NTX mixed with HA1 or HA3b compared with stimulation with NTX. The percentage of CD3 cells remained unchanged. These results suggest strongly that HA1 and HA3b demonstrate adjuvant activity via increasing IL6 production.

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  • HLA-DQA1*0103-DQB1*0601 haplotype and Helicobacter pylori-positive gastric mucosa-associated lymphoid tissue lymphoma Reviewed

    Yoshiro Kawahara, Motowo Mizuno, Tadashi Yoshino, Kenji Yokota, Keiji Oguma, Hiroyuki Okada, Shigeatsu Fujiki, Yasushi Shiratori

    Clinical Gastroenterology and Hepatology   3 ( 9 )   865 - 868   2005.9

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    Background &amp
    Aims: Immune responses to Helicobacter pylori are important in the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In this retrospective case study, we investigated whether certain alleles and haplotypes of major histocompatibility complex genes are associated with gastric MALT lymphoma and the efficacy of H pylori eradication therapy on the lymphoma. Methods: Blood samples were obtained from 18 patients with H pylori-positive gastric MALT lymphoma (5 men and 13 women
    age range, 51-80 years), 30 patients with H pylori-positive non-ulcer dyspepsia (17 men and 13 women
    age range, 37-77 years), and 30 patients with H pylori-negative non-ulcer dyspepsia (12 men and 18 women
    age range, 37-77 years). HLA-DQA1 and DQB1 allele typing was performed by use of a polymerase chain reaction sequence-specific oligonucleotide procedure. All patients with MALT lymphoma were treated with H pylori eradication therapy and followed up by repeated endoscopy and biopsy. Results: We found a significant increase in alleles HLA-DQA1*0103 and HLA-DQB1*0601, and a haplotype DQA1*0103-DQB1*0601, in MALT lymphoma patients when compared with non-ulcer dyspepsia patients who were either H pylori-positive or not and with a healthy control population. After H pylori eradication, the lymphomas regressed completely in all 10 patients who possessed the DQA1*0103-DQB1*0601 haplotype but in only 4 of the 8 without this haplotype (P = .023). Conclusions: DQA1*0103-DQB1*0601 haplotype-positive gastric MALT lymphoma is likely to respond to therapy by eradication of H pylori. © 2005 by the American Gastroenterological Association.

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  • The effect of eradicating Helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease Reviewed

    Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Kenji Yokota, Keiji Oguma, Hiroyuki Okada, Yasushi Shiratori

    American Journal of Gastroenterology   100 ( 5 )   1037 - 1042   2005.5

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    OBJECTIVES: Infection with Helicobacter pylori is a risk factor for the development of gastric cancer. However, it is not known whether eradication therapy can prevent the development of gastric cancer in persons in whom the cancer is not yet established. In the present study, we investigated whether the eradication of H. pylori in patients with peptic ulcer disease reduces the likelihood of their developing gastric cancer. METHODS: Prospective posteradication evaluations were conducted in 1,342 consecutive patients (1,191 men and 151 women
    mean age: 50 yr) with peptic ulcer diseases who had received H. pylori eradication therapy. After confirmation of eradication, endoscopy and a urea breath test were performed yearly. RESULTS: A total of 1,120 patients completed more than 1-yr follow-up and were followed for up to 8.6 yr (a mean of 3.4 yr). Gastric cancer developed in 8 of 944 patients cured of infection and 4 of 176 who had persistent infection (p = 0.04
    log-rank test). All the gastric cancer developed in patients with gastric ulcer, but none in patients with duodenal ulcer (p = 0.005
    Fisher's exact test). In patients with gastric ulcer, persistent infection was identified as a significant factor for the risk of developing gastric cancer (hazard ratio: 3.35
    95% confidence interval: 1.00-11.22
    p = 0.04
    Cox's proportional-hazards model). CONCLUSION: H. pylori eradication may reduce their risk of developing gastric cancer in patients with gastric ulcer. Large-scale studies in additional populations of this important international public-health issue are warranted. © 2005 by Am. Coll. of Gastroenterology Published by Blackwell Publishing.

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  • Neutrophil and lymphocyte responses to oral Streptococcus in Adamantiades-Behcet's disease Reviewed

    T Kurauchi, K Yokota, T Matsuo, Y Fujinami, E Isogai, H Isogai, H Ohtsuki, K Oguma

    FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY   43 ( 2 )   125 - 131   2005.2

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    Immune reactions against microorganisms play an important pathogenic role in Adamantiades-Behcet's disease. We had previously obtained Streptococcus sanguinis (strain BD 113-20), isolated from the oral cavity of patients with Adamantiades-Behcet's syndrome. To investigate the pathogenesis of this isolate, we examined neutrophil reactions and levels of cytokine production by lymphocytes after stimulation with the strain. The reactions of neutrophils were examined by chemiluminescence assay using whole blood. The amounts of interferon gamma (IFN-gamma) and interleukin (IL)-4, IL-8, IL-10 and IL-12, produced by peripheral blood mononuclear cells, were measured by ELISA. Strain BD113-20 activated neutrophils from Adamantiades-Behcet's patients and healthy volunteers, and, in addition it increased the IFN-gamma production by lymphocytes. Lymphocytes from Adamantiades-Behcet's patients showed a dominant T helper-1 immune response. Results indicated that both bacterial stimulation and host hypersensitivity might be involved in the symptoms and pathogenesis of Adamantiades-Behcet's disease. (C) 2004 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.

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  • Alteration in the composition of cholesteryl glucosides and other lipids in Helicobacter pylori undergoing morphological change from spiral to coccoid form Reviewed

    Hirofumi Shimomura, Shunji Hayashi, Kenji Yokota, Keiji Oguma, Yoshikazu Hirai

    FEMS Microbiology Letters   237 ( 2 )   407 - 413   2004.8

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    In this analysis of membrane lipid compositions in Helicobacter pylori, the membrane lipid profiles drastically changed during coccoid formation: cholesteryl-6-O-tetradecanoyl-α-D-glucopyranoside levels increased, cholesteryl-α-D-glucopyranoside and phosphatidyl ethanolamine decreased, and a coordinated increase in cardiolipin and decrease in phosphatidyl glycerol were observed. Cholesteryl-6-O-phosphatidyl-α-D-glucopyranoside was hardly detected in the spiral forms in the logarithmic phase, but subsequently increased throughout the coccoid conversion. These results suggest that environmental stresses induce the expression of certain regulatory systems for lipid metabolism in H. pylori, and that the resulting alterations in lipid composition play an important role in inducing the coccoid conversion. © 2004 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.

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  • Helicobacter pylori Eradication Improves Pre-Existing Reflux Esophagitis in Patients With Duodenal Ulcer Disease Reviewed

    Kuniharu Ishiki, Motowo Mizuno, Susumu Take, Yasuhiro Nagahara, Tomowo Yoshida, Kazuhide Yamamoto, Hiroyuki Okada, Kenji Yokota, Keiji Oguma, Yasushi Shiratori

    CLINICAL GASTROENTEROLOGY AND HEPATOLOGY   2 ( 6 )   474 - 479   2004.6

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    Background & Aims: There has been significant controversy over the relationship between Helicobacter pylori infection and reflux esophagitis. We investigated the effects of eradicating H. pylori on the reflux esophagitis found in patients with peptic ulcers. Methods: Prospective posteradication evaluations were conducted yearly in 162 H. pylori-positive patients who had reflux esophagitis together with peptic ulcer disease (4 women and 158 men, mean age = 49.1 yr). The Los Angeles classification of the patients' esophagitis was: grade A, 90; grade B, 63; and grade C, 9. The follow-up evaluations began 1 to 2 months after completion of the eradication treatment (mean time of follow-up = 22 mo), and consisted of endoscopy and an interview focusing on heartburn. Results: Six patients were withdrawn from the study because of adverse drug reactions or a failure to regularly keep their appointments. After eradication therapy, we observed endoscopically that reflux esophagitis had improved in 87 (55.8%) of the 156 patients. The improvement rate was significantly higher in patients cured of infection (60.8%) than in those with persistent H. pylori infection (38.9%) (P = 0.04). Body mass index (odds ratio = 0.86, 95% confidence interval [CI] = 0.76-0.97), cure of infection (3.68, 95% CI = 1.56-8.69), the absence of a hiatal hernia (3.90, 95% CI = 1.83-8.28), and an ulcer located in the duodenum (2.75, 95% CI = 1.33-5.70) were identified as significant independent factors for the improvement of reflux esophagitis. Conclusions: In patients with reflux esophagitis associated with duodenal ulcer, a significant improvement in pre-existing reflux esophagitis was noted after H. pylori eradication.

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  • Antibody to heat shock protein can be used for early serological monitoring of Helicobacter pylori eradication treatment Reviewed

    N Yunoki, K Yokota, M Mizuno, Y Kawahara, M Adachi, H Okada, S Hayashi, Y Hirai, K Oguma, T Tsuji

    CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY   7 ( 4 )   574 - 577   2000.7

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    Infection with Helicobacter pylori induces humoral immune responses against various antigens of the bacterium. Heat shock proteins (hsps) are immunodominant antigens in various diseases including H. pylori infection. In the present study, we measured the anti-hsp antibody titers in 42 patients with H. pylori-infected peptic ulcers during a bacterial eradication study. The patients were treated with a proton pump inhibitor and antimicrobial agents to eradicate the organism. Their sera were obtained at pretreatment and at 1 month and 6 months after the eradication therapy. The titers of immunoglobulin G antibodies to the H. pylori hsp, whole-cell lysate, and urease (30-kDa subunit) antigens in serum were measured by a capture enzyme-linked immunosorbent assay. The levels of H. pylori hsp60 antibodies in sera collected 1 month after treatment had declined significantly, even when changes in the titers of antibodies to whole-cell and urease antigens were not apparent. These results suggest that measurement of antibodies to H. pylori hsp60 in serum is useful far the early monitoring of the effectiveness of eradication therapy.

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  • Combined effect of rebamipide and ecabet sodium on Helicobacter pylori adhesion to gastric epithelial cells Reviewed

    S Hayashi, T Sugiyama, K Yokota, H Isogai, E Isogai, H Shimomura, K Oguma, N Asaka, Y Hirai

    MICROBIOLOGY AND IMMUNOLOGY   44 ( 7 )   557 - 562   2000

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    Helicobacter pylori is a major etiological agent in gastroduodenal disorders. The adhesion of H, pylori to gastric epithelial cells is the initial step of N, pylori infection. Inhibition of H, pylori adhesion is thus a therapeutic target in the prevention of H, pylori infection. me have reported that rebamipide and ecabet sodium, mucoprotective antiulcer agents, independently inhibit H. pylori adhesion. However, the antiadhesion activity of each antiulcer agent was incomplete. Experiments were performed to evaluate the combined effect of rebamipide and ecabet sodium on H, pylori adhesion to gastric epithelial cells, MKN-28 and MKN-45 cells, derived from human gastric carcinomas, were used as target cells, Twelve clinical isolates of H, pylori were used in this study. We evaluated the effects of rebamipide and ecabet sodium, individually and in combination, on H. pylori adhesion to target cells quantitatively using our previously established enzyme-linked immunosorbent assay. Rebamipide and ecabet sodium each partially inhibited H. pylori adhesion. In contrast, adhesion was almost completely inhibited by pretreating target cells and N, pylori with the combination of rebamipide and ecabet sodium, Our studies suggest that the synergistic antiadhesion activity of rebamipide and ecabet sodium is greater than that of each antiulcer agent alone.

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  • Characterization of haemagglutinin activity of Clostridium botulinum type C and D 16S toxins, and one subcomponent of haemagglutinin (HA1)

    Kaoru Inoue, Yukako Fujinaga, Koichi Honke, Kenji Yokota, Tetsuya Ikeda, Tohru Ohyama, Kouichi Takeshi, Toshihiro Watanabe, Katsuhiro Inoue, Keiji Oguma

    Microbiology   145 ( 9 )   2533 - 2542   1999

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    The 16S toxin and one subcomponent of haemagglutinin (HA), designated HA1, were purified from a type D culture of Clostridium botulinum by a newly established procedure, and their HA activities as well as that of purified type C 16S toxin were characterized. SDS-PAGE analysis indicated that the free HA1 forms a polymer with a molecular mass of approximately 200 kDa. Type C and D 16S toxins agglutinated human erythrocytes in the same manner. Their HA titres were dramatically reduced by employing erythrocytes that had been previously treated with neuraminidase, papain or proteinase K, and were inhibited by the addition of N-acetylneuraminic acid to the reaction mixtures. In a direct-binding test to glycolipids such as SPG (NeuAcα2-Galβ1-4GlcNAcβ1-3Galβ1-4Glcβ1-Cer) and GM3 (NeuAcα2-3Galβ1-4Glcβ1-Cer), and glycoproteins such as glycophorin A and/or B prepared from the erythrocytes, both toxins bound to sialylglycolipids and sialoglycoproteins, but bound to neither neutral glycolipids nor asialoglycoproteins. On the basis of these results, it was concluded that type C and D 16S toxins bind to erythrocytes through N-acetylneuraminic acid. HA1 showed no haemagglutination activity, although it did bind to sialylglycolipids. We therefore speculate that binding to glycoproteins rather than to glycolipids may be important in causing haemagglutination by type C and D 16S toxins.

    DOI: 10.1099/00221287-145-9-2533

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  • Antibody and cytokine responses in Helicobacter-pylori-infected various mouse strains Reviewed

    A Dey, K Yokota, K Kosavashi, K Oguma, Y Hirai, T Akagi

    ACTA MEDICA OKAYAMA   52 ( 1 )   41 - 48   1998.2

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    Helicobacter pylori (H. pylori) infection in the stomach is etiologically closely associated with chronic active gastritis, peptic ulcer, gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma. In this study, we examined the antibody responses and cytokine profiles of three strains of mice (BALB/c, C3H/He, and C57BL/6) infected with H. pylori. Following this, correlations between host-immune reactions and intensity of inflammation were analyzed. H. pylori (ATCC43504) was intragastrically administered once a week to the mice from 4 weeks of age, and they were sacrificed at the ages of 4 and 7 months. In these mice, we examined the histology of the stomach, antibody titers against H. pylori, and serum levels of cytokines (IL-4, IL-10, TNF-alpha, IL-2 and Interferon-gamma). In BALB/c mice, inflammation of the stomach was minimal. Inflammation was observed in 63.6% of C57BL/6 mice and 33.3% of C3H/He mice. In C57BL/6 and C3H/He mice, all the cytokines tended to increase, In contrast, BALB/c mice were inactive in cytokine production except for IL-2, Two C3H/He mice developed severe inflammation with lymph follicles; one showed a response largely typical of Th-1, and the other showed a response largely typical of Th-2. Although a definite correlation was not shown between Th-1/Th-2 response evaluated by cytokine production and intensity of inflammation, it appears that in H. pylori-induced inflammation both cell-mediated (Th-1) and humoral (Th-2) immunity play a role in pathogenesis.

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  • Analysis of immunoglobulin A antibodies to Helicobacter pylori in serum and gastric juice in relation to mucosal inflammation Reviewed

    Hayashi, S, Sugiyama, T, Yokota, K, Isogai, H, Isogai, E, Oguma, K, Asaka, M, Fujii, N, Hirai, Y

    Clin. Diag. Labo. Immunol.   5 ( 5 )   617 - 621   1998

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  • IgA protease produced by Streptococcus sanguis and antibody production against IgA protease in patients with Behcet's disease Reviewed

    K Yokota, K Oguma

    MICROBIOLOGY AND IMMUNOLOGY   41 ( 12 )   925 - 931   1997

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    The production of IgA protease in twelve strains of Streptococcus sanguis isolated from patients with Behcet's disease (BD) was examined, Protease activity was detected in 10 out of 12 strains, The protease was purified from one representative strain, S. sanguis 113-20, by employing Rotofor and DEAE-Sephacel chromatography, The molecular mass of the purified protease was approximately 100 kDa, and it cleaved the proline-threonine site of the IgA, Both IgG and IgA titers against the cells (113-20) and the purified IgA protease in the sera of BD patients and healthy controls, 36 each, were assayed, The IgG titers against the cells and protease were not significant in the BD patients or controls, but the IgA titers against the cells and protease in the BD patients were significantly higher than those of the controls, These data indicate that the BD patients are infected with IgA protease-producing S. sanguis strains, which cause an increase of IgA titer against these organisms and IgA protease antigen. Since the organisms can proliferate in BD patients for a long period of time (years), it seems that IgA antibodies cannot effectively eliminate the organisms.

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  • 80 尋常性乾癬患者におけるCandida albicans血中抗体価の特徴と時間的推移について

    田中 智, 山本 美保, 飯田 憲治, 松田 三千雄, 林 俊治, 横田 憲治, 小熊 恵二

    アレルギー   45 ( 8 )   900 - 900   1996

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    DOI: 10.15036/arerugi.45.900_4

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  • LIPID PROFILES OF HELICOBACTER-PYLORI AND HELICOBACTER-MUSTELAE GROWN IN SERUM-SUPPLEMENTED AND SERUM-FREE MEDIA Reviewed

    M HAQUE, Y HIRAI, K YOKOTA, K OGUMA

    ACTA MEDICA OKAYAMA   49 ( 4 )   205 - 211   1995.8

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    Many of Helicobacter species have been found to have novel cholesteryl glucosides (CGs). To study the biosynthetic mechanism of CGs, the lipid profiles of H. pylori and H. mustelae grown in serum-supplemented and cholesterol-restricted serum-free media were investigated. In contrast to the serum-supplemented state, helicobacters had less CGs in the serum-free state; a trace amount of CGs and no CG was detected in H. pylori and H. mustelae, respectively. The proportion of total and individual phospholipid also showed significant alteration. Unknown lipids which did not contain phosphate and sugar were detected in the serum-free state, but not in the serum-supplemented state. The CGs were found to be distributed mainly in the membrane fractions, and one of the unknown lipids was found exclusively in the cytosol fraction. Based on these data,it is apparent that the CGs of helicobacters are synthesized by de novo uptake of cholesterol from the media. The unknown lipids detected in the serum-free state may be storage lipids, appearing in response to depletion of nutrients, especially cholesterol, or other factors in the media.

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  • 240 尋常性乾癬におけるCandida albicans血中抗体価の検討

    田中 智, 飯田 憲治, 松田 三千雄, 林 俊治, 続 佳代, 横田 憲治, 小熊 恵二

    アレルギー   44 ( 3 )   414 - 414   1995

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    DOI: 10.15036/arerugi.44.414_4

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  • 231 アトピー性皮膚炎におけるCandida albicans血中抗体価の検討

    飯田 憲治, 田中 智, 林 俊治, 続 佳代, 松田 三千雄, 横田 憲治, 小熊 恵二

    アレルギー   44 ( 3 )   412 - 412   1995

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    DOI: 10.15036/arerugi.44.412_3

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  • HELICOBACTER-PYLORI INDUCES INFLAMMATION IN MOUSE URINARY-BLADDER AND PELVIS Reviewed

    H ISOGAI, E ISOGAI, K KIMURA, N FUJII, K YOKOTA, K OGUMA

    MICROBIOLOGY AND IMMUNOLOGY   38 ( 5 )   331 - 336   1994

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    Helicobacter pylori was transurethrally inoculated into the mouse urinary tract. The organism established infection and induced inflammation in the urinary bladder and pelvis. During the infection, urinary pH was elevated, probably due to the production of NH3 by bacterial urease. H. pylori was recovered from the urinary bladder, kidney and urine of the infected mice. Histopathologically, severe neutrophil infiltration was observed in the mucosal layer of both organs. H. pylori was detected on the surface of the epithelial cells. These results indicate that low pH and bacterial flora were not essential factors in establishing the mucosal infection with H. pylori. This experimental system is useful to investigate the pathogenicity of H. pylori in mucosal organs.

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  • Heat Shock Protein Produced by Helicobacter pylori

    Yokota Kenji, Hirai Yoshikazu, Haque Mahmudul, Hayashi Shyunji, Isogai Hiroshi, Sugiyama Toshiro, Nagamachi Eiko, Tsukada Yutaka, Fujii Nobuhiro, Oguma Keiji

    Japanese Journal of Microbiology   38 ( 5 )   403 - 405   1994

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    The cells of Helicobacter pylori were suspended in the medium containing 35S-methionine. After a heat shock of the cells at 42C for 5, 10, and 30min, the production of proteins was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. Out of many proteins produced by the cells, only 66kDa protein production was dramatically increased by heat treatment. The N-terminal amino acid sequence of 66kDa protein was quite similar to that of 62kDa and 54kDa proteins previously suggested as heat shock protein (HSP) of H. pylori based on the reaction with polyclonal and monoclonal antibodies against HSP 60 family proteins produced by other bacteria. Therefore, it was concluded that H. pylori produces the 66kDa protein as its major heat shock protein which belongs to HSP 60 family.

    DOI: 10.1111/j.1348-0421.1994.tb01799.x

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  • 356 アトピー性皮膚炎におけるCandida albicans血中抗体価の検討

    飯田 憲治, 田中 智, 横田 憲治, 小熊 恵二, 松田 三千雄

    アレルギー   42 ( 9 )   1398 - 1398   1993

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    DOI: 10.15036/arerugi.42.1398_2

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  • Antibody Response to Oral Streptococci in Behçet's Disease

    YOKOTA Kenji, HAYASHI Syunji, FUJII Nobuhiro, YOSHIKAWA Kouji, KOTAKE Satoshi, ISOGAI Emiko, OHNO Shigeaki, ARAKI Yoshio, OGUMA Keiji

    Japanese Journal of Microbiology   36 ( 8 )   815 - 822   1992

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    The serum antibody titers against oral streptococci were studied by enzyme-linked immunosorbent assay (ELISA) both in patients with Behçet's disease (BD) and control groups. The patients with BD showed significantly higher antibody titers to S. sanguis strains 113-20, 114-23, and 118-1 which were isolated from patients with BD, in comparison with control groups. Also, the reactions of high-titered sera to the crude cell wall and soluble (or membrane) fractions of the 113-20 strain were observed by western blot test. The sera of the patients with BD demonstrated strong bands of approximately 36kDa, 82kDa, and 87kDa in the crude cell wall fractions, and many bands of 80kDa to 150kDa in the membrane fractions, indicating that these proteins are the ones leading the high antibody titers to this bacterium in the sera of patients with BD.

    DOI: 10.1111/j.1348-0421.1992.tb02083.x

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  • 胃壁中のCampylobacter pyloriの同定法の検討と血中抗菌抗体の測定 Reviewed

    横田憲治, 小熊恵二, 吉田博清, 高山義一, 杉山敏郎, 矢花 剛, 谷内 昭, 榑林陽一, 磯貝 浩, 磯貝恵美子

    感染症学会誌   64   597 - 603   1990

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    DOI: 10.11150/kansenshogakuzasshi1970.64.597

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  • 尿沈渣標本中に出現する顆粒状物質と尿路感染症細菌との関連について

    佐藤 妃映, 横田 憲治, 渡辺 朱理, 苔口 進, 衛藤 友美, 高阪 翔士

    日本環境感染学会総会プログラム・抄録集   33回   297 - 297   2018.2

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  • 環境汚染菌の消毒剤および除菌洗浄剤含浸ワイプによる拭き取り除去効果

    横田 憲治, 渡邉 都貴子, 林 俊治, 渡辺 朱理, 苔口 進, 平井 義一, 松下 治

    日本防菌防黴学会誌   46 ( 1 )   3 - 8   2018.1

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    近年、環境汚染菌による院内感染が報告され、環境整備の重要性が認められつつある。今回、消毒剤および除菌剤の除染効果を比較検討するため、環境中の細菌の生存状態とATP測定の基礎的検討と各種消毒剤または除菌剤を含浸させたワイプによる拭き取り効果について検討した。乾燥による生菌数への影響に関する検討では、一定の濃度に調製した多剤耐性Acinetobacter baumanniiおよびBacillus cereusを乾燥状態で放置し、経時的に細菌数の指標としてATP値とコロニー数を計測した。シャーレの中で乾燥状態にしたB.cereusは1日目でATP値が有意に低下したが、A.baumanniiは有意な低下を認めるまでに7日間を要した。7日目のコロニー数を計測したところ、A.baumanniiおよびB.cereus共に生菌として検出された。拭き取りによる除菌効果は、ステンレス板とポリプロピレン板にA.baumanniiおよびB.cereusを塗布し、上記消毒剤または除菌剤含浸ワイプで拭き取り、その前後におけるATP量およびコロニー数を比較検討した。拭き取り効果は、材質による差は認められなかった。また、いずれの含浸ワイプによる拭き取りにおいても同様に有意な菌数の低下が認められ、いずれの細菌に対しても消毒剤または除菌剤は5log10CFU以上の減少を認めた。(著者抄録)

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  • 環境汚染菌の消毒剤および除菌洗浄剤含浸ワイプによる拭き取り除去効果

    横田 憲治, 渡邉 都貴子, 林 俊治, 渡辺 朱理, 苔口 進, 平井 義一, 松下 治

    日本防菌防黴学会誌   46 ( 1 )   3 - 8   2018.1

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    近年、環境汚染菌による院内感染が報告され、環境整備の重要性が認められつつある。今回、消毒剤および除菌剤の除染効果を比較検討するため、環境中の細菌の生存状態とATP測定の基礎的検討と各種消毒剤または除菌剤を含浸させたワイプによる拭き取り効果について検討した。乾燥による生菌数への影響に関する検討では、一定の濃度に調製した多剤耐性Acinetobacter baumanniiおよびBacillus cereusを乾燥状態で放置し、経時的に細菌数の指標としてATP値とコロニー数を計測した。シャーレの中で乾燥状態にしたB.cereusは1日目でATP値が有意に低下したが、A.baumanniiは有意な低下を認めるまでに7日間を要した。7日目のコロニー数を計測したところ、A.baumanniiおよびB.cereus共に生菌として検出された。拭き取りによる除菌効果は、ステンレス板とポリプロピレン板にA.baumanniiおよびB.cereusを塗布し、上記消毒剤または除菌剤含浸ワイプで拭き取り、その前後におけるATP量およびコロニー数を比較検討した。拭き取り効果は、材質による差は認められなかった。また、いずれの含浸ワイプによる拭き取りにおいても同様に有意な菌数の低下が認められ、いずれの細菌に対しても消毒剤または除菌剤は5log10CFU以上の減少を認めた。(著者抄録)

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  • 歯科予防処置における飛散汚染状況調査 ATP測定法と細菌培養法からの検討

    渡辺 朱理, 苔口 進, 横田 憲治, 松山 美和

    日本歯科衛生学会雑誌   12 ( 1 )   145 - 145   2017.8

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  • Beyondボノプラザン標準療法 当院における3次除菌療法(PPI/P-CAB+AMPC+STFX)とペニシリンアレルギーに対する治療成績の検討

    榮 浩行, 横田 憲治, 大林 由佳, 河野 吉泰, 三浦 公, 岡田 裕之

    日本ヘリコバクター学会学術集会プログラム・抄録集   23回   90 - 90   2017.6

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  • H.pylori感染胃炎の内視鏡診断の進歩 H.pylori除菌後再感染は、内視鏡所見で診断できるか?

    大林 由佳, 武 進, 榮 浩行, 河野 吉泰, 三浦 公, 楠本 智章, 横田 憲治, 水野 元夫, 岡田 裕之

    日本ヘリコバクター学会学術集会プログラム・抄録集   23回   109 - 109   2017.6

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  • エアロゾルサンプルからの非結核性抗酸菌の分離検出

    平井 一行, 横田 憲治, 平井 義一

    日本環境感染学会総会プログラム・抄録集   32回   257 - 257   2017.2

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  • 細菌性コラゲナーゼのマトリックス・アンカーの構造解析と骨新生誘導のための複合剤開発(Structural analysis of a matrix anchor in bacterial collagenase to develop an osteogenic therapeutic)

    松下 治, 内田 健太郎, 関口 裕之, 美間 健彦, 後藤 和義, 山本 由弥子, 横田 憲治, 高相 晶士, Bauer Ryan, Sakon Joshua

    日本細菌学雑誌   72 ( 1 )   109 - 109   2017.2

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  • Vibrio alginolyticusのコラゲナーゼ発現はHapRにより調節される(Expression of colA is regulated by HapR in Vibrio alginolyticus)

    美間 健彦, 西川 裕太郎, 中田 悠介, 波多野 直哉, 後藤 和義, 山本 由弥子, 横田 憲治, 松下 治

    日本細菌学雑誌   72 ( 1 )   106 - 106   2017.2

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  • 腸肝在位Helicobacter感染症研究の最前線 肝胆道系疾患とヘパティカス菌感染

    横田 憲治

    日本細菌学雑誌   72 ( 1 )   32 - 32   2017.2

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  • Vibrio alginolyticusのコラゲナーゼ発現はHapRにより調節される(Expression of colA is regulated by HapR in Vibrio alginolyticus)

    美間 健彦, 西川 裕太郎, 中田 悠介, 波多野 直哉, 後藤 和義, 山本 由弥子, 横田 憲治, 松下 治

    日本細菌学雑誌   72 ( 1 )   106 - 106   2017.2

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  • 病院内環境におけるメチシリン耐性ブドウ球菌調査

    渡辺 朱理, 横田 憲治, 苔口 進, 松山 美和

    日本歯科衛生学会雑誌   11 ( 1 )   152 - 152   2016.8

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  • 合成コラーゲン様基剤とコラーゲン結合型線維芽細胞増殖因子を用いた複合剤による骨形成促進法の開発

    濱本 奈々, 内田 健太郎, 関口 裕之, 美間 健彦, 後藤 和義, 山本 由弥子, 横田 憲治, 高相 晶士, 松下 治

    日本細菌学雑誌   71 ( 1 )   126 - 126   2016.2

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  • Vibrio alginolyticus I.029のコラゲナーゼ発現はHapRにより調節される

    西川 裕太郎, 美間 健彦, 中田 悠介, 後藤 和義, 山本 由弥子, 横田 憲治, 松下 治

    日本細菌学雑誌   71 ( 1 )   127 - 127   2016.2

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  • 口腔内におけるメトロニダゾール耐性歯周病細菌の調査

    苔口 進, 渡辺 朱理, 横田 憲治

    日本環境感染学会誌   31 ( Suppl. )   478 - 478   2016.2

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  • 歯ブラシへの付着・残存口腔内細菌調査

    長瀬 優里, 苔口 進, 横田 憲治, 松山 美和, 渡辺 朱理

    四国公衆衛生学会雑誌   61 ( 1 )   87 - 92   2016.2

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    歯ブラシは使用の度に口腔内細菌が付着し、残存する。不潔な歯ブラシを使用することによって、齲蝕や口臭などの原因になることも報告されている。本研究は歯ブラシを清潔かつ衛生的に使用し、管理するという意識の向上に繋げることを目的とした。すなわち、1ヵ月間連続使用した歯ブラシに付着・残存する口腔内細菌数を調べて、同時に毛先の形態変化も確認した。さらに歯ブラシの使用条件や保管方法の違いによる歯ブラシに付着・残存した口腔内細菌数も比較した。1ヵ月間連続使用した歯ブラシには1.0×10^8CFUの口腔内細菌が付着・残存しており、毛先の広がりとともに歯ブラシへの付着・残存口腔内細菌の増加が認められた。また歯ブラシの使用条件による比較では、歯ブラシへの付着・残存していた口腔内細菌数にほとんど差はなく、保管方法ではケースに保管した場合に口腔内細菌が最も多く残存していた。今回の調査から1ヵ月間連続使用した歯ブラシの衛生状態は悪く、毛先の広がりや摩耗が口腔内細菌数の蓄積や残存の増加に影響していると考えられるため、定期的な交換が必要であろう。また湿潤状態が長く続く保管環境では、歯ブラシの付着・残存細菌数は増加していたので、歯ブラシの適切な保管方法が重要であると考える。(著者抄録)

    DOI: 10.15053/2016.11.04

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  • Examination of the Antimicrobial and Cleaning Effects of Commercially Available Soaps

    YOSHIDA Yoko, WATANABE Tokiko, HAYASHI Shunji, HIRAI Yoshikazu, YOKOTA Kenji

    40 ( 11 )   685 - 691   2012.11

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  • THERAPEUTIC POSSIBILITY FOR PATIENTS WITH BEHCET&apos;S DISEASE BY THE PEPTIDES OF HEAT SHOCK PROTEIN-65/60 DERIVED FROM ORAL STREPTOCOCCI

    Fumio Kaneko, Ari Togashi, Noritaka Oyama, Koichiro Nakamura, Emiko Isogai, Kenji Yokota, Keiji Oguma

    CLINICAL AND EXPERIMENTAL RHEUMATOLOGY   28 ( 4 )   S119 - S119   2010.7

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  • ROLE OF ORAL STREPTOCOCCI IN THE PATHOGENESIS OF BEHCET&apos;S DISEASE

    Fumio Kaneko, Noritaka Oyama, Hirokatsu Yanagihori, Emiko Isogai, Kenji Yokota, Keiji Oguma

    CLINICAL AND EXPERIMENTAL RHEUMATOLOGY   26 ( 4 )   S16 - S16   2008.7

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  • Eradication of Helicobacter pylori before the significant expansion of mucosal atrophy is most beneficial to prevent gastric cancer

    Motowo Mizuno, Susumu Take, Yasuhiro Nagahara, Kuniharu Ishiki, Tomowo Yoshida, Kenji Yokota, Keiji Oguma

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY   22   A63 - A63   2007.10

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  • H. pylori-抗原刺激によるマンノースレセプターファミリーDEC205のマクロファージでの発現

    藤本 聖人, 横田 憲治, 趙 瑩, 綾田 潔, 小熊 惠二

    日本細菌学雑誌   62 ( 1 )   169 - 169   2007.2

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  • ヘリコバクター・ピロリのフラボドキシン代謝におけるクラスC酸性ホスファターゼの関与

    下村 裕史, 林 俊治, 横田 憲治, 小熊 恵二, 平井 義一

    日本細菌学雑誌   62 ( 1 )   87 - 87   2007.2

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  • Vibrio vulnificus 弱毒化株のマウス感染実験におけるワクチン効果

    瀬川 理恵, 井上 美幸, 横田 憲治, 小熊 惠二, 山本 耕一郎

    日本細菌学雑誌   62 ( 1 )   172 - 172   2007.2

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  • 署名Tagトランスポゾン挿入変異法による Vibrio vulnificus 弱毒化変異株の分離

    細原 浩平, 瀬川 理恵, 光原 沙織, 菅 悠喜, 横田 憲治, 小熊 惠二, 山本 耕一郎

    日本細菌学雑誌   62 ( 1 )   126 - 126   2007.2

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  • ベーチェット病における炎症に関与している細菌抗原の解析

    申 蓮花, 横田 憲治, 綾田 潔, 阪口 義彦, 平井 一行, 長町 栄子, 小熊 惠二

    日本細菌学雑誌   62 ( 1 )   74 - 74   2007.2

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  • 胆汁検体よりの Helicobacter 属の存在確認と培養の試み

    横田 憲治, 綾田 潔, 阪口 義彦, 藤本 聖人, 長町 榮子, 小熊 惠二

    日本細菌学雑誌   62 ( 1 )   179 - 179   2007.2

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  • Behcet病発症における細菌抗原の意義 (第1土曜特集 Behcet病--病因の解明と難治性病態の克服に向けて) -- (病因・病態)

    横田 憲治, 小熊 惠二

    医学のあゆみ   215 ( 1 )   19 - 22   2005.10

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  • H. cinaedi, H. fenneliae, H. pullorum の性状と病原性

    平井 義一, 下村 裕史, 林 俊治, 横田 憲治, 小熊 恵二

    臨床と微生物 = Clinical microbiology   32 ( 2 )   175 - 180   2005.3

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  • ボツリヌスB型神経毒素に結合している無毒成分の免疫増強作用について

    李 在哲, 横田 憲治, 崔 錦花, 有満 秀幸, 阪口 義彦, 藤永 由佳子, 金 英姫, 松村 拓大, 株本 祐子, 小熊 恵二

    日本細菌学雑誌   59 ( 1 )   282 - 282   2004.2

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  • 胃MALTリンパ腫に対するHelicobacter pylori(HP)除菌療法後の経過とsecond line治療としての放射線療法へのタイミング

    岡田裕之, 水野元夫, 白鳥康史, 吉野 正, 横田憲治

    消化器科   38,1,53-58   2004

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  • 臨床 H.pyloriのゲノムと病原性 (特集 微生物ゲノム情報と医学--基礎と臨床)

    林 俊治, 平井 義一, 横田 憲治

    現代医療   34 ( 5 )   1091 - 1096   2002

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  • H. pylori感染と胃粘膜免疫応答.

    横田憲治, 綾田 潔, 石井栄子, 山崎理恵, 小林計太, 吉野 正, 林 俊治, 平井義一, 赤木忠厚, 小熊恵二

    日本臨床   59,342-348   2001

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  • CAP18(抗菌および抗エンドトキシン蛋白)の生体防御因子としての役割

    平田陸正, 切替照雄, 横田憲治, 田村弘志, 田中重則, 小熊恵二, 佐藤成大

    日本細菌学雑誌   55 ( 2 )   347   2000.4

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    J-GLOBAL

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  • The Bacteriocidal Effect of the Electrolysed Functioning Water against Helicobacter pylori

    NAKAO Miyuki, YOKOTA Kenji, OGUMA Keiji, TAKAI Kenichi

    74 ( 2 )   120 - 127   2000.2

  • Treatment of Helicobacter pylori infection

    Hayashi, S, Hirai, Y, Isogai, H, Isogai, E, Yokota, K, Oguma, K

    Res. Adv. Antimicrob. Chemother.   1   7 - 12   2000

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  • H. pyloriの胃リンパ腫への関与

    吉野 正, 赤木忠厚, 横田憲治, 小熊恵二, 河原祥朗

    癌の臨床   46:839-845   2000

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  • Association of Helicobacter pylori with gastroduodenal diseases

    Y Hirai, S Hayashi, H Shimomura, K Oguma, K Yokota

    JAPANESE JOURNAL OF INFECTIOUS DISEASES   52 ( 5 )   183 - 197   1999.10

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    Helicobacter pylori was first cultured in vitro in 1982. This bacterium is a spiral gram negative rod which grows under microaerophilic conditions. The ecological niche is the mucosa of the human stomach which had been thought to be aseptic before the discovery of this bacterium. This organism causes a long-lasting infection throughout a person's life if there is no medical intervention. Numerous persons are infected with the organism around the world, and the rate of infection in Japan is nearly 50% of the population. However, the route of infection remains unclear because the organism has not been isolated from any environment other than several animals. H. pylori is now recognized as a causative agent of gastritis and peptic ulcers. Though gastritis, and especially chronic active gastritis, is observed at least histologically in all persons with H. pylori, peptic ulcers develop in only some infected persons. Specific factors in the host and/or the bacteria are needed for the development of peptic ulcer disease. Furthermore, H. pylori is considered to be related to the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma, especially those of low grade. Also, H. pylori infection is a major determinant for initiating the sequence of events leading to gastric cancer. In some patients with low-grade gastric MALT lymphoma, the eradication of H. pylori led to a regression of lesion. Gastric cancer has been induced in Mongolian gerbils with long-term H. pylori infection. The combinations of drugs, which consist of an antisecretory agent (acid-supressing agent) and antimicrobial agents, are used for the eradication of the organism. Eradication therapy is recommended at least for patients with peptic ulcers.

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  • ボツリヌスprogenitor toxinのHAサブコンポーネントの小腸微絨毛及び赤血球への結合活性について

    藤永 由佳子, 井上 薫, 横田 憲治, 長町 榮子, 小熊 惠二

    日本細菌学雑誌   54 ( 1 )   117 - 117   1999.2

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  • Helicobacter pyloriのHSP60の発現と生物活性の検討

    横田 憲治, 石井 栄子, 綾田 潔, 平井 義一, 林 俊治, 藤永 由佳子, 小熊 惠二

    日本細菌学雑誌   54 ( 1 )   212 - 212   1999.2

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  • 岡山県における腸管出血性大腸菌O157:H7の分子疫学的検討

    船守 有香, 横田 憲治, 藤永 由佳子, 井上 薫, 小熊 惠二

    日本細菌学雑誌   54 ( 1 )   203 - 203   1999.2

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  • Helicobacter pyloriのワクチン療法 (特集 Helicobacter pyloriの基礎と臨床)

    小熊 恵二, 横田 憲治, 平井 義一

    診断と治療   86 ( 1 )   89 - 94   1998.1

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    Other Link: http://search.jamas.or.jp/link/ui/1998108533

  • Effect of ecabet sodium on Helicobacter pylori adhesion to gastric epithelial cells

    HAYASHI Shunji, SUGIYAMA Toshiro, YACHI Akira, YOKOTA Kenji, HIRAI Yoshikazu, OGUMA Keiji, FUJII Nobuhiro

    32 ( 5 )   593 - 597   1997.10

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  • ボツリヌス神経毒素-無毒成分複合体の構造と機能

    井上 薫, 藤永 由佳子, 横田 憲治

    蛋白質核酸酵素   42 ( 13 )   2049 - 2060   1997.10

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  • Helicobacter pylori and gastroduodenal disease

    K Yokota, Y Hirai, K Oguma

    JAPANESE JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH   42 ( 3 )   193 - 209   1996.6

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    Helicobacter pylori is a gram negative spiral bacterium, which is colonized in human gastric mucosa. This organism was first reported in Australia, 1983. Now H. pylori has been recognized to cause chronic active gastritis, and is a major factor in the pathogenesis of duodenal ulcer and gastric ulcer. It was also reported that its infection is a risk factor for both MALT (mucosa associated lymphoid tissue) lymphoma and gastric adenocarcinoma.
    H. pylori has many virulence factors. Urease is one of the most important colonization and virulence factors studied. Ammonia made by urease protects the organisms from gastric low pH, and is toxigenic to gastric epithelial cells. Vacuolating toxin and CagA proteins are thought to be pathogenic agents especially for causing gastric and duodenal ulcers. Neutrophil reactions against the bacteria, and the abnormal immunological reactions are also considered to cause the damage of gastric epithelial cells, although the detailed pathogenic mechanisms are still not clear.
    In developing countries, infection by H. pylori is established in childhood, and the organisms can be identified in the mouth and feces, indicating its infection through water.
    The infected organisms can be eradicated by administration with proton pump inhibitor and one or two antibiotics. This may provide an useful therapeutic means to the patients especially with recurrent ulceration and MALT lymphoma.

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  • スナネズミおよびマウスを用いる感染実験モデル. Helicobacter pylori と胃粘膜障害

    磯貝 浩, 磯貝恵美子, 横田憲治, 小熊恵二

    日本臨床   51   3183 - 3143   1993

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  • Development and Evaluation of Capture Enzyme-Linked Immunosorbent Assays for Detection of Immunoglobulin G and M Antibodies to Group A Streptococcal Antigens

    Hayashi Shunji, Yokota Kenji, Takizawa Yoshihiko, Tomizawa Isao, Nejime Tetsuya, Oguma Keiji

    Japanese Journal of Microbiology   37 ( 4 )   271 - 279   1993

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    Capture enzyme-linked immunosorbent assays (ELISAs) were developed to detect immunoglobulin G and M antibodies to group A streptococcal (GAS) antigens, streptolysin O, streptokinase, and group A carbohydrate. The sensitivities and the specificities of the IgM capture ELISAs to each GAS antigen were high enough to distinguish the patients with GAS infections (diagnosed as GAS pharyngitis or scarlet fever) from the control groups (healthy people and patients with pharyngitis from whom GAS could not be isolated). On the other hand, the specificities of the IgG capture ELISAs were not very effective in diagnosis of GAS infections. When the capture ELISA and an indirect ELISA detecting IgM antibodies to group A carbohydrate were compared, false-positive reactions due to rheumatoid factor occurred in the indirect ELISA, but did not occur in the capture ELISA. These results indicate that the capture ELISA works better than the indirect ELISA in detecting the IgM antibody, and that the IgM capture ELISA to GAS antigen provides a rapid and highly reliable serodiagnosis for GAS infections employing only a single serum.

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  • Fundamental Microbiology (2020academic year) Third semester  - 水4,水5

  • Genetics (2020academic year) 3rd and 4th semester  - [第3学期]水6,水7, [第4学期]火1,火2

  • Genetics (2020academic year) 3rd and 4th semester  - [第3学期]水6,水7, [第4学期]火1,火2

  • Genetics (2020academic year) 3rd and 4th semester  - [第3学期]水6,水7, [第4学期]火1,火2

  • Genetics (2020academic year) 3rd and 4th semester  - [第3学期]水6,水7, [第4学期]火1,火2

  • Infection and Immunity (2020academic year) 1st semester  - 水2,水3

  • Infection and Immunity (2020academic year) 1st semester  - 水2,水3

  • Infection and Immunity (2020academic year) 1st semester  - 水2,水3

  • Infection and Immunity (2020academic year) 1st semester  - 水2,水3

  • Infection and Immunity (2020academic year) 1st semester  - 水2,水3

  • Infection and Immunity (2020academic year) 1st semester  - 水2,水3

  • Seminar in Analysis of Infectious Diseases and Pathogenic Factors (2020academic year) Late  - 水7

  • Topics in Analysis of Infectious Diseases and Pathogenic Factors (2020academic year) Prophase  - 水7

  • Calamity Crisis Management Theory (2020academic year) Summer concentration  - その他

  • Calamity Crisis Management Theory (2020academic year) Summer concentration  - その他

  • Calamity Crisis Management Theory (2020academic year) Summer concentration  - その他

  • Seminar in Analysis of Pathogenic Factors (2020academic year) Late  - 木1

  • Topics in Analysis of Pathogenic Factors (2020academic year) Prophase  - 木1

  • Thesis Research on Pathophysiology (2020academic year) Year-round  - その他

  • Pathological Information Analysis Science Special Research (2020academic year) Year-round  - その他

  • Practical Training in Medical Technology (2020academic year) 1st-4th semester  - その他

  • Scientific study (2020academic year) special  - その他

  • Clinical Microbiology (2020academic year) Third semester  - 木4,木5

  • Laboratory Exercise in Clinical Microbiology (2020academic year) Fourth semester  - 水3~8,木3~8

  • Clinical Pharmacology (2020academic year) Second semester  - 火3,火4,金3,金4

  • Introduction course for Health Sciences (2020academic year) Prophase  - 水5

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