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The interplay between host immune cells and gut microbiota in chronic inflammatory diseases
김동현,Melody Y Zeng,Gabriel Núñez 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Many benefits provided by the gut microbiota to the host rely on its intricate interactions with host cells. Perturbations of the gut microbiota, termed gut dysbiosis, affect the interplay between the gut microbiota and host cells, resulting in dysregulation of inflammation that contributes to the pathogenesis of chronic inflammatory diseases, including inflammatory bowel disease, multiple sclerosis, allergic asthma and rheumatoid arthritis. In this review, we provide an overview of how gut bacteria modulates host metabolic and immune functions, summarize studies that examined the roles of gut dysbiosis in chronic inflammatory diseases, and finally discuss measures to correct gut dysbiosis as potential therapeutics for chronic inflammatory diseases.
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Kim, Donghyun,Seo, Sang-Uk,Zeng, Melody Y.,Kim, Wan-Uk,Kamada, Nobuhiko,Inohara, Naohiro,Nú,ú,ñ,ez, Gabriel The American Association of Immunologists, Inc. 2017 JOURNAL OF IMMUNOLOGY Vol.199 No.4
<P>Enteric pathogens including Salmonella enteric serovar Typhimurium can breach the epithelial barrier of the host and spread to systemic tissues. In response to infection, the host activates innate immune receptors via the signaling molecule MyD88, which induces protective inflammatory and antimicrobial responses. Most of these innate immune responses have been studied in hematopoietic cells, but the role of MyD88 signaling in other cell types remains poorly understood. Surprisingly, we found that Dermo1-Cre;Myd88(fl/fl) mice with mesenchymal cell-specific deficiency of MyD88 were less susceptible to orogastric and i.p. S. Typhimurium infection than their Myd88(fl/fl) littermates. The reduced susceptibility of Dermo1-Cre; Myd88(fl/fl) mice to infection was associated with lower loads of S. Typhimurium in the liver and spleen. Mutant analyses revealed that S. Typhimurium employs its virulence type III secretion system 2 to promote its growth through MyD88 signaling pathways in mesenchymal cells. Inflammatory monocytes function as a major cell population for systemic dissemination of S. Typhimurium. Mechanistically, mesenchymal cell-specific MyD88 signaling promoted CCL2 production in the liver and spleen and recruitment of inflammatory monocytes to systemic organs in response to S. Typhimurium infection. Consistently, MyD88 signaling in mesenchymal cells enhanced the number of phagocytes including Ly6C(hi)Ly6G(-) inflammatory monocytes harboring S. Typhimurium in the liver. These results suggest that S. Typhimurium promotes its systemic growth and dissemination through MyD88 signaling pathways in mesenchymal cells.</P>
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