第95回日本細菌学会総会

講演情報

ワークショップ

[W2] ワークショップ2
口腔感染症の新しい病因論

2022年3月30日(水) 09:15 〜 11:45 チャンネル2

コンビーナー:吉田 明弘(松本歯科大学),今井 健一(日本大学)

[W2-4] 口腔細菌叢の乱れが招く腸炎の増悪メカニズム

北本 祥,鎌田 信彦 (ミシガン大・医・消化器内科)

Given the previous studies demonstrating the association between oral and gut disease in a clinical setting, it is conceivable that there may be a causative link, particularly between oral and gut inflammation. In this context, we recently revealed that periodontal inflammation exacerbates gut inflammation in vivo. The translocation of oral pathobionts expanded in the inflamed oral cavity to the gut activates the inflammasome in colonic mononuclear phagocytes, thereby triggering inflammation. In parallel, oral pathobiont-reactive Th17 cells generated in the oral cavity upon periodontitis are imprinted with gut tropism and migrate to the inflamed gut. Once in the gut, Th17 cells of oral origin can be activated by translocated oral pathobionts and cause the development of colitis. Thus, oral inflammation, such as periodontitis, exacerbates gut inflammation by supplying the gut with both colitogenic pathobionts and pathogenic T cells. Collectively, these findings highlight the causal role of oral dysbiosis driven by inflammation in the development of gut inflammation via the complex intermucosal connection between the mouth and gut.