第94回日本細菌学会総会

講演情報

シンポジウム

[S4] 病原細菌と宿主免疫の鬩ぎ合い

2021年3月24日(水) 09:15 〜 11:45 チャンネル1

コンビーナー:久堀 智子(岐阜大学大学院医学系研究科),日吉 大貴(長崎大学熱帯医学研究所)

[S4-3] Helicobacter pyloriによる宿主脂質の病原因子への変換

○山崎 晶 (阪大・微研・分子免疫制御)

Helicobacter pylori (H. 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 non-canonical 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.