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.

口腔感染导致口腔外疾病发病机理的确切机制仍不清楚。在这里，我们报道牙周炎症会在体内加剧肠道炎症。牙周炎导致口腔病原菌的扩大，包括克雷伯菌和肠杆菌种，在口腔中。摄入大量麻痹的口腔类生物体，并转移至肠道，在那里它们激活结肠单核吞噬细胞中的炎症小体，从而引发炎症。同时，牙周炎导致在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细胞具有肠道嗜性印记，并迁移至发炎的肠道。当进入肠道时，口腔来源的Th17离子可激活口腔来源的Th17细胞，并引起结肠炎的发展，但肠道内的微生物不会激活它们。因此，口腔炎症，例如牙周炎，通过向肠道供应致病性致病菌和致病性T细胞，加剧了肠道炎症。