The Intermucosal Connection between the Mouth and Gut in Commensal Pathobiont-Driven Colitis
The Intermucosal Connection between the Mouth and Gut in Commensal Pathobiont-Driven Colitis
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DOI：
10.1016/j.cell.2020.05.048
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发表时间：
2020-07-23
期刊：
影响因子：
64.5
通讯作者：
Kamada, Nobuhiko
中科院分区：
文献类型：
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作者：
Kitamoto, Sho;Nagao-Kitamoto, Hiroko;Kamada, Nobuhiko
口腔感染导致口腔外疾病发病的确切机制尚不清楚。在这里，我们报告说，牙周炎症加剧肠道炎症在体内。牙周炎导致口腔致病菌（包括克雷伯氏菌属和肠杆菌属物种）在口腔中的扩张。积聚的口腔病原体被摄入并移位到肠道，在那里它们激活结肠单核吞噬细胞中的炎性体，引发炎症。同时，牙周炎导致口腔中产生口腔病原体反应性Th17细胞。口腔病原体反应性Th17细胞具有肠道向性并迁移到发炎的肠道。当在肠道中时，口腔来源的Th17细胞可以被易位的口腔致病菌激活并导致结肠炎的发展，但它们不会被肠道驻留的微生物激活。因此，口腔炎症，如牙周炎，通过向肠道提供大肠杆菌致病菌和致病性T细胞而加剧肠道炎症。
The precise mechanism by which oral infection contributes to the pathogenesis of extra-oral diseases remains unclear. Here, we report that periodontal inflammation exacerbates gut inflammation in vivo. Periodontitis leads to expansion of oral pathobionts, including Klebsiella and Enterobacter species, in the oral cavity. Amassed oral pathobionts are ingested and translocate to the gut, where they activate the inflammasome in colonic mononuclear phagocytes, triggering inflammation, In parallel, periodontitis results in generation of oral pathobiont-reactive Th17 cells in the oral cavity. Oral pathobiont-reactive Th17 cells are imprinted with gut tropism and migrate to the inflamed gut. When in the gut, Th17 cells of oral origin can be activated by translocated oral pathobionts and cause development of colitis, but they are not activated by gut-resident microbes. Thus, oral inflammation, such as periodontitis, exacerbates gut inflammation by supplying the gut with both colitogenic pathobionts and pathogenic T cells.