論文

査読有り 国際誌
2021年1月4日

Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors.

The Journal of experimental medicine
  • Masahiro Nagata
  • ,
  • Kenji Toyonaga
  • ,
  • Eri Ishikawa
  • ,
  • Shojiro Haji
  • ,
  • Nobuyuki Okahashi
  • ,
  • Masatomo Takahashi
  • ,
  • Yoshihiro Izumi
  • ,
  • Akihiro Imamura
  • ,
  • Koichi Takato
  • ,
  • Hideharu Ishida
  • ,
  • Shigenori Nagai
  • ,
  • Petr Illarionov
  • ,
  • Bridget L Stocker
  • ,
  • Mattie S M Timmer
  • ,
  • Dylan G M Smith
  • ,
  • Spencer J Williams
  • ,
  • Takeshi Bamba
  • ,
  • Tomofumi Miyamoto
  • ,
  • Makoto Arita
  • ,
  • Ben J Appelmelk
  • ,
  • Sho Yamasaki

218
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記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1084/jem.20200815

Helicobacter pylori causes gastritis, which has been attributed to the development of H. pylori-specific T cells during infection. However, the mechanism underlying innate immune detection leading to the priming of T cells is not fully understood, as H. pylori evades TLR detection. Here, we report that H. pylori metabolites modified from host cholesterol exacerbate gastritis through the interaction with C-type lectin receptors. Cholesteryl acyl α-glucoside (αCAG) and cholesteryl phosphatidyl α-glucoside (αCPG) were identified as noncanonical ligands for Mincle (Clec4e) and DCAR (Clec4b1). During chronic infection, H. pylori-specific T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial burdens remained unchanged. Furthermore, a mutant H. pylori strain lacking αCAG and αCPG exhibited an impaired ability to cause gastritis. Thus H. pylori-specific modification of host cholesterol plays a pathophysiological role that exacerbates gastric inflammation by triggering C-type lectin receptors.

リンク情報
DOI
https://doi.org/10.1084/jem.20200815
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32991669
ID情報
  • DOI : 10.1084/jem.20200815
  • PubMed ID : 32991669

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