Faculty Profiles - YOKOTA Kenji

MISC - YOKOTA Kenji

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ROLE OF ORAL STREPTOCOCCI IN THE PATHOGENESIS OF BEHCET'S DISEASE

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

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

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

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

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

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

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

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

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

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

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

Helicobacter pylori heat-shock protein 60 induces production of the pro-inflammatory cytokine IL8 in monocytic cells

SN Lin, K Ayada, Y Zhao, K Yokota, R Takenaka, H Okada, R Kan, S Hayashi, M Mizuno, Y Hirai, Y Fujinami, K Oguma

JOURNAL OF MEDICAL MICROBIOLOGY 54 ( 3 ) 225 - 233 2005.3

Language：English Publisher：SOC GENERAL MICROBIOLOGY

Interleukin 8 (IL8) is usually produced in both epithelial and monocytic cells during bacterial infections, causing inflammation. Helicobacter pylori induces production of IL8 from gastric epithelial cells via its cag pathogenicity island (cag PAI) system, LPS and outer-membrane protein. In some bacteria, heat-shock protein 60 (HSP60) also elicits a strong pro-inflammatory response in cells of the innate immune system. Three recombinant H. pylori HSP60 (rHSP60) proteins of different sizes were produced and one of these was used to raise two monoclonal antibodies (2E7 and 7135). IL8 production was found to be induced in cultured monocytic cells treated with H. pylori cells or rHSP60 proteins, as measured by ELISA, and the amount of IL8 produced was dose-dependent. Pre-incubation of H. pylori cells or rHSP60 preparations with the antibody 2E7 significantly inhibited IL8 production from monocytic cells. These results indicated that HSP60 is closely associated with IL8 production in monocytic cells.

DOI： 10.1099/jmm.0.45871-0

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Mechanisms of inflammation induced by H. pylori-HSP60

Kenji Yokota, Kiyoshi Ayada, Son-NanLin, Keiji Oguma, Ryuta Takenaka

Nippon rinsho. Japanese journal of clinical medicine 63 75 - 79 2005

Helicobacter pylori heat-shock protein 60 induces inflammatory responses through the toll-like receptor-triggered pathway in cultured human gastric epithelial cells

R Takenaka, K Yokota, K Ayada, M Mizuno, Y Zhao, Y Fujinami, SN Lin, T Toyokawa, H Okada, Y Shiratori, K Oguma

MICROBIOLOGY-SGM 150 3913 - 3922 2004.12

Language：English Publisher：SOC GENERAL MICROBIOLOGY

Contact between Helicobacter pylori and gastric epithelial cells results in activation of NF-kappaB followed by secretion of interleukin (IL)-8. However, host-cell receptor(s) and their ligands involved in H. pylori-related IL-8 production have yet to be fully defined. In this study, the interaction between Toll-like receptors (TLRs), which are host receptors for pathogens involved in the innate immune response, and heat-shock protein (HSP) 60, an immune-potent antigen of H. pylori, was examined during H. pylori-induced IL-8 secretion in vitro. Recombinant H. pylori HSP60 (rHpHSP60) was prepared and added to cultured KATO III human gastric epithelial cells with or without pre-incubation with mouse monoclonal anti-TLR2 or anti-TLR4 antibodies. IL-8 mRNA expression and IL-8 protein release were analysed by Northern blotting and immunoassay. Involvement of NF-kappaB activation was analysed immunocytochemically by anti-NF-kappaB p65 antibody and ammonium pyrrolidinedithiocarbamate (PDTC), an inhibitor of NF-kappaB-mediated transcriptional activation. rHpHSP60 induced IL-8 mRNA expression and IL-8 secretion in a dose-dependent manner in KATO III cells. Anti-TLR2 antibody inhibited rHpHSP60-induced IL-8 secretion by 75%, and anti-TLR4 antibody inhibited it by 30%. rHpHSP60 induced nuclear translocation of NF-kappaB p65, which was inhibited by pretreatment with anti-TLR2 antibody. Treatment with PDTC significantly decreased the secretion of IL-8 induced by rHpHSP60. These findings suggest that H. pylori HSP60 activates NF-kappaB and induces IL-8 production through TLR-triggered pathways in gastric epithelial cells. Thus, it is possible that H. pylori HSP60 and TLR interaction in host cells contributes to the development of gastric inflammation caused by H. pylori infection.

DOI： 10.1099/mic.0.27527-0

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Serum antibodies to Helicobacter pylori and its heat shock protein 60 correlate with the response of gastric mucosa-associated lymphoid tissue lymphoma to eradication of H. pylori

R Takenaka, H Okada, M Mizuno, C Makidono, SI Hori, A Fujiwara, T Yoshino, K Yokota, K Oguma, Y Shiratori

GASTROENTEROLOGY 126 ( 4 ) A181 - A181 2004.4

Characterization of elongated Helicobacter pylori isolated from a patient with gastric-mucosa-associated lymphoid-tissue lymphoma

T Toyokawa, K Yokota, M Mizuno, Y Fujinami, R Takenaka, H Okada, S Hayashi, Y Hirai, K Oguma, Y Shiratori

JOURNAL OF MEDICAL MICROBIOLOGY 53 ( 3 ) 207 - 212 2004.3

Language：English Publisher：SOC GENERAL MICROBIOLOGY

To date, two Helicobacter species, Helicobacter pylori and 'Helicobacter heilmanni' (formerly named 'Gastrospirillum hominis'), have been identified from the human stomach. In this study, we observed non-H. pylori-shaped bacteria in gastric tissue sections and successfully isolated them by cultivation. Elongated bacteria were isolated from a patient with gastric-mucosa-associated lymphoid-tissue lymphoma who had been diagnosed as H. pylori-negative by culture, rapid urease test and histopathology in another hospital. The bacteria were grown only on chocolate agar in a CO2 incubator, appeared more than 10 mum long in histological sections, formed small colonies and showed poor growth in a brain heart infusion broth; these characteristics apparently differed from common clinical isolates of H. pylori. However, the bacteria were identified as H. pyloriby PCR of the urease gene, 16S rDNA sequencing, protein profile and antigenicity examined by anti-H. pylori polyclonal antibody. These observations suggest that the H. pylori strain identified in this study may contribute to the development of gastroduodenal diseases in cases judged as H. pylori-negative by ordinary methods.

DOI： 10.1099/jmm.0.05281-0

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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

Immune response in Helicobacter pylori-induced low-grade gastric-mucosa-associated lymphoid tissue (MALT) lymphoma

R Yamasaki, K Yokota, H Okada, S Hayashi, M Mizuno, T Yoshino, Y Hirai, D Saitou, T Akagi, K Oguma

JOURNAL OF MEDICAL MICROBIOLOGY 53 ( 1 ) 21 - 29 2004.1

Language：English Publisher：SOC GENERAL MICROBIOLOGY

We have reported previously that heat-shock protein 60 kDa (hsp60) of Helicobacter pylori is an important antigen in the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In order to investigate associations with host immune reactions and hsp60 antigen, CD40 ligand (CD40L) expression and cytokine production were analysed following stimulation with hsp60. To provide a clear antigen-driven immune response, peripheral blood mononuclear cells (PBMC) from patients with low-grade MALT lymphoma and gastritis and those from healthy volunteers were stimulated with recombinant H. pylori hsp60 and H. pylori cell lysate in the presence of cytokines (IL4 and granulocyte-macrophage colony-stimulating factor). mRNA expression was also analysed by a cDNA microarray containing 1100 genes. Expression of CD40L on PBMCs of patients with MALT lymphoma was increased by cytokines or by combination with stimulation with hsp60 antigens. The production of IL4 in PBMC cultures was increased in patients with MALT lymphoma; however, production of IFN-gamma was at low levels. DNA microarray analysis indicated increased levels of HLA-DR and integrin mRNAs. In cases of low-grade MALT lymphoma, adaptive immune responses against hsp60 may be enhanced by host factors, such as antigen presentation and T-cell activation, resulting in B-cell proliferation, which can be demonstrated during chronic H. pylori infection.

DOI： 10.1099/jmm.0.05348-0

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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

神経変性疾患髄液中の抗Helicobacter pylori heat shock protein 60抗体の検出

齊藤正樹, 千葉進, 青木雅俊, 松本博之, 杉山敏郎, 藤永由佳子, 横田憲治, 藤浪良仁, 小熊恵二

臨床神経学 43 ( 12 ) 1069 - 1069 2003.12

Heat shock protein 60 of Helicobacter pylori induces inflammatory responses through the toll-like receptor-triggered pathway in cultured human gastric epithelial cells

R Takenaka, K Yokota, M Mizuno, Y Fujinami, T Toyokawa, S Hiraoka, S Hori, C Makidono, S Take, H Okada, K Oguma, Y Shiratori

GASTROENTEROLOGY 124 ( 4 ) A590 - A590 2003.4

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