文献

J-GLOBAL ID：202102243446708473   整理番号：21A0349177

Helicobacter pylori代謝産物はC型レクチン受容体を介して胃炎を悪化させる【JST・京大機械翻訳】

Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors

著者 (34件)： Nagata Masahiro (Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan) ,  Toyonaga Kenji (Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan) ,  Ishikawa Eri (Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan) ,  Ishikawa Eri (Laboratory of Molecular Immunology, Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan) ,  Haji Shojiro (Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan) ,  Haji Shojiro (Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan) ,  Okahashi Nobuyuki (Department of Bioinformatics Engineering, Graduate School of Information Science and Technology, Osaka University, Suita, Osaka, Japan) ,  Okahashi Nobuyuki (Laboratory for Metabolomics, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan) ,  Takahashi Masatomo (Division of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Fukuoka, Japan) ,  Izumi Yoshihiro (Division of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Fukuoka, Japan) ,  Imamura Akihiro (Department of Applied Bioorganic Chemistry, Gifu University, Gifu, Gifu, Japan) ,  Takato Koichi (Department of Applied Bioorganic Chemistry, Gifu University, Gifu, Gifu, Japan) ,  Ishida Hideharu (Department of Applied Bioorganic Chemistry, Gifu University, Gifu, Gifu, Japan) ,  Ishida Hideharu (Center for Highly Advanced Integration of Nano and Life Sciences (G-CHAIN), Gifu University, Gifu, Gifu, Japan) ,  Nagai Shigenori (Department of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan) ,  Illarionov Petr (School of Biosciences, University of Birmingham, Birmingham, UK) ,  Stocker Bridget L. (School of Chemical and Physical Sciences, Victoria University of Wellington, Wellington, New Zealand) ,  Stocker Bridget L. (Centre for Biodiscovery, Victoria University of Wellington, Wellington, New Zealand) ,  Stocker Bridget L. (Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand) ,  Timmer Mattie S.M. (School of Chemical and Physical Sciences, Victoria University of Wellington, Wellington, New Zealand) ,  Timmer Mattie S.M. (Centre for Biodiscovery, Victoria University of Wellington, Wellington, New Zealand) ,  Timmer Mattie S.M. (Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand) ,  Smith Dylan G.M. (School of Chemistry and Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, Victoria, Australia) ,  Williams Spencer J. (School of Chemistry and Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, Victoria, Australia) ,  Bamba Takeshi (Division of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Fukuoka, Japan) ,  Miyamoto Tomofumi (Department of Natural Products Chemistry, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Fukuoka, Japan) ,  Arita Makoto (Laboratory for Metabolomics, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan) ,  Arita Makoto (Cellular and Molecular Epigenetics Laboratory, Graduate School of Medical Life Science, Yokohama City University, Yokohama, Kanagawa, Japan) ,  Arita Makoto (Division of Physiological Chemistry and Metabolism, Graduate School of Pharmaceutical Sciences, Keio University, Minato-ku, Tokyo, Japan) ,  Appelmelk Ben J. (Molecular Microbiology/Medical Microbiology and Infection Control, Amsterdam University Medical Centers, Amsterdam, Netherlands) ,  Yamasaki Sho (Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan) ,  Yamasaki Sho (Laboratory of Molecular Immunology, Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan) ,  Yamasaki Sho (Division of Molecular Design, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Fukuoka, Japan) ,  Yamasaki Sho (Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan)
資料名： Journal of Experimental Medicine  (Journal of Experimental Medicine)
巻： 218  号： 1  ページ： Null  発行年： 2020年 
JST資料番号： A0937B  ISSN： 0022-1007  資料種別： 逐次刊行物 (A)
記事区分： 原著論文  発行国： アメリカ合衆国 (USA)  言語： 英語 (EN)

抄録/ポイント： Helicobacter pyloriは胃炎を引き起こし,感染時のH.pylori特異的T細胞の発生に起因する。しかし,T細胞のプライミングをもたらす自然免疫検出の根底にある機構は,H.pyloriがTLRを検出するので,完全には理解されていない。ここでは,宿主コレステロールから変性したH.pylori代謝産物がC型レクチン受容体との相互作用を介して胃炎を悪化させることを報告する。コレステリルアシルα-グルコシド(αCAG)とコレステリルホスファチジルα-グルコシド(αCPG)を,Mincle(Clec4e)とDCAR(Clec4b1)の非標準リガンドとして同定した。慢性感染の間,H.pylori特異的T細胞反応と胃炎は,Mincle欠損マウスで改善したが,細菌負荷は不変であった。さらに,αCAGとαCPGを欠く変異体H.pylori株は胃炎を引き起こす障害能力を示した。したがって,宿主コレステロールのH.pylori特異的修飾はC型レクチン受容体を誘発することにより胃炎症を悪化させる病態生理学的役割を果たす。Please refer to the version of record for the copyright holder. Translated from English into Japanese by JST.【JST・京大機械翻訳】

シソーラス用語： 相互作用 ,  *代謝産物 ,  T細胞 ,  *胃炎 ,  *Helicobacter pylori ,  自然免疫 ,  リガンド ,  C型レクチン受容体 ,  Mincle ,  *微生物 ,  *らせん菌 ,  ステロール ,  脂環式アルコール
準シソーラス用語： 慢性化 , 【Automatic Indexing@JST】

分類 (4件)： 消化器の基礎医学  (GH01020E) ,  感染症・寄生虫症一般  (GD01010H) ,  微生物感染の生理と病原性  (EG03053T) ,  感染免疫  (ED03030P)

物質索引 (1件)： コレステロール

引用文献 (60件)：

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タイトルに関連する用語 (5件)： Helicobacter ,  代謝産物 ,  C型レクチン受容体 ,  胃炎 ,  悪化