Cell：牙周炎“坏细菌”加剧肠道炎症的双重机制
- ①牙周炎症可加剧小鼠的肠道炎症；
- ②牙周炎导致口腔中的致病共生菌增多，包括多种克雷伯菌属和肠杆菌属细菌；
- ③这些大量积累的致病共生菌可被摄入并在发炎的肠道内异位定植，激活结肠单核吞噬细胞的炎性体介导的IL-1β生成，增加炎症反应；
- ④另一方面，牙周炎可诱导在口腔中产生与口腔致病共生菌反应的Th17细胞；
- ⑤结肠炎期间，这些Th17细胞可迁移至发炎的肠道，被移位至肠道的口腔致病共生菌激活，加重肠道炎症。
主编推荐语
越来越多的研究显示，口腔中的致病共生菌可能是一些疾病（特别是肠道疾病）的重要诱因和帮凶。《Cell》最新发表的一项研究发现，牙周炎导致的口腔致病共生菌增多，能加剧结肠炎。一方面，这些“坏细菌”在口腔炎症时大量积累，可移位到发炎的肠道中定植下来，直接增加肠道的炎症反应；另一方面，牙周炎发生时，这些菌还能通过诱导能迁移至肠道的致病性Th17细胞，来间接加剧肠道炎症。这些发现说明，口腔和肠道在菌群和免疫两个层面上都是紧密相连的，保护肠道健康一定不能忽视口腔健康。
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The Intermucosal Connection between the Mouth and Gut in Commensal Pathobiont-Driven Colitis
致病共生菌驱动的结肠炎中的口腔和肠道的粘膜间连接
10.1016/j.cell.2020.05.048
2020-06-16, Article
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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.
First Authors:
Sho Kitamoto
Correspondence Authors:
Nobuhiko Kamada
All Authors:
Sho Kitamoto,Hiroko Nagao-Kitamoto,Yizu Jiao,Merritt G Gillilland III,Atsushi Hayashi,Jin Imai,Kohei Sugihara,Mao Miyoshi,Jennifer C Brazil,Peter Kuffa,Brett D Hill,Syed M Rizvi,Fei Wen,Shrinivas Bishu,Naohiro Inohara,Kathryn A Eaton,Asma Nusrat,Yu L Lei,William V Giannobile,Nobuhiko Kamada
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