The Intermucosal Connection between the Mouth and Gut in Commensal Pathobiont-Driven Colitis.

Autor:	Kitamoto S; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Nagao-Kitamoto H; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Jiao Y; Department of Pathology, University of Michigan, Ann Arbor, MI, USA; Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI, USA., Gillilland MG 3rd; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Hayashi A; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA; Research Laboratory, Miyarisan Pharmaceutical Co., Ltd., Tokyo, Japan., Imai J; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Sugihara K; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Miyoshi M; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Brazil JC; Department of Pathology, University of Michigan, Ann Arbor, MI, USA., Kuffa P; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Hill BD; Department of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA., Rizvi SM; Department of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA., Wen F; Department of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA., Bishu S; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA., Inohara N; Department of Pathology, University of Michigan, Ann Arbor, MI, USA., Eaton KA; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, USA., Nusrat A; Department of Pathology, University of Michigan, Ann Arbor, MI, USA., Lei YL; Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI, USA., Giannobile WV; Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI, USA., Kamada N; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA. Electronic address: nkamada@umich.edu.
Jazyk:	angličtina
Zdroj:	Cell [Cell] 2020 Jul 23; Vol. 182 (2), pp. 447-462.e14. Date of Electronic Publication: 2020 Jun 16.
DOI:	10.1016/j.cell.2020.05.048
Abstrakt:	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. Competing Interests: Declaration of Interests The authors declare no competing interests. (Copyright © 2020 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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