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      An orally administered oral pathobiont and commensal have comparable and innocuous systemic effects in germ-free mice

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          Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells.

          Commensal microbes can have a substantial impact on autoimmune disorders, but the underlying molecular and cellular mechanisms remain largely unexplored. We report that autoimmune arthritis was strongly attenuated in the K/BxN mouse model under germ-free (GF) conditions, accompanied by reductions in serum autoantibody titers, splenic autoantibody-secreting cells, germinal centers, and the splenic T helper 17 (Th17) cell population. Neutralization of interleukin-17 prevented arthritis development in specific-pathogen-free K/BxN mice resulting from a direct effect of this cytokine on B cells to inhibit germinal center formation. The systemic deficiencies of the GF animals reflected a loss of Th17 cells from the small intestinal lamina propria. Introduction of a single gut-residing species, segmented filamentous bacteria, into GF animals reinstated the lamina propria Th17 cell compartment and production of autoantibodies, and arthritis rapidly ensued. Thus, a single commensal microbe, via its ability to promote a specific Th cell subset, can drive an autoimmune disease. Copyright 2010 Elsevier Inc. All rights reserved.
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            Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia: the "red complex", a prototype polybacterial pathogenic consortium in periodontitis.

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              Polymicrobial synergy and dysbiosis in inflammatory disease.

              Uncontrolled inflammation of the periodontal area may arise when complex microbial communities transition from a commensal to a pathogenic entity. Communication among constituent species leads to polymicrobial synergy between metabolically compatible organisms that acquire functional specialization within the developing community. Keystone pathogens, even at low abundance, elevate community virulence, and the resulting dysbiotic community targets specific aspects of host immunity to further disable immune surveillance while promoting an overall inflammatory response. Inflammophilic organisms benefit from proteinaceous substrates derived from inflammatory tissue breakdown. Inflammation and dysbiosis reinforce each other, and the escalating environmental changes further select for a pathobiotic community. We have synthesized the polymicrobial synergy and dysbiotic components of the process into a new model for inflammatory diseases.
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                Author and article information

                Journal
                Journal of Periodontal Research
                J Periodont Res
                Wiley
                00223484
                December 2018
                December 2018
                July 26 2018
                : 53
                : 6
                : 950-960
                Affiliations
                [1 ]Research Unit for Oral-Systemic Connection; Division of Oral Science for Health Promotion; Niigata University Graduate School of Medical and Dental Sciences; Niigata Japan
                [2 ]Division of Periodontology; Niigata University Graduate School of Medical and Dental Sciences; Niigata Japan
                [3 ]Department of Periodontology; Tokyo Dental College; Tokyo Japan
                Article
                10.1111/jre.12593
                © 2018

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