The Journal of experimental medicine · 2021
Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors.
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Nagata Masahiro, Toyonaga Kenji, Ishikawa Eri, Haji Shojiro, Okahashi Nobuyuki, Takahashi Masatomo, Izumi Yoshihiro, Imamura Akihiro, Takato Koichi, Ishida Hideharu, Nagai Shigenori, Illarionov Petr, Stocker Bridget L, Timmer Mattie S M, Smith Dylan G M, Williams Spencer J, Bamba Takeshi, Miyamoto Tomofumi, Arita Makoto, Appelmelk Ben J, Yamasaki Sho
Аннотация
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.