Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors

Masahiro Nagata, Kenji Toyonaga, Eri Ishikawa, Shojiro Haji, Nobuyuki Okahashi, Masatomo Takahashi, Yoshihiro Izumi, Akihiro Imamura, Koichi Takato, Ishida 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. AppelmelkSho Yamasaki

研究成果: Article査読

40 被引用数 (Scopus)


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 a-glucoside (aCAG) and cholesteryl phosphatidyl a-glucoside (aCPG) 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 aCAG and aCPG 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.

ジャーナルJournal of Experimental Medicine
出版ステータスPublished - 2021 1月 4

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学


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