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      Discordance between changes in the gut microbiota and pathogenicity in a mouse model of spontaneous colitis

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          Abstract

          Under conventional conditions, mice deficient in core 1-derived O-glycans (TM-IEC C1galt1 −/−), which have a defective mucus layer, experienced spontaneous inflammation of the colon. Analysis of fecal bacterial populations by pyrosequencing of 16S rRNA gene showed that disease in conventional TM-IEC C1galt1 −/− was associated with shifts in the microbiota manifested by increases in Lactobacillus and Clostridium species, and decreases in unclassified Ruminococcaceae and Lachnospiraceae. Under germ-free (GF) conditions, TM-IEC C1galt1 −/− presented decreased goblet cells, but did not develop inflammation. Monoassociation of GF TM-IEC C1galt1 −/− revealed that bacterial species differ significantly in their ability to induce inflammatory changes. Bacteroides thetaiotaomicron caused inflammation, while Lactobacillus johnsonii (enriched during colitis) did not. These observations demonstrate that not all microbiota shifts that correlate with disease contribute to pathogenesis.

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          Commensal anaerobic gut bacteria attenuate inflammation by regulating nuclear-cytoplasmic shuttling of PPAR-gamma and RelA.

          Denise Kelly, Jamie I D Campbell, Timothy P King … (2004)
          The human gut microflora is important in regulating host inflammatory responses and in maintaining immune homeostasis. The cellular and molecular bases of these actions are unknown. Here we describe a unique anti-inflammatory mechanism, activated by nonpathogenic bacteria, that selectively antagonizes transcription factor NF-kappaB. Bacteroides thetaiotaomicron targets transcriptionally active NF-kappaB subunit RelA, enhancing its nuclear export through a mechanism independent of nuclear export receptor Crm-1. Peroxisome proliferator activated receptor-gamma (PPAR-gamma), in complex with nuclear RelA, also undergoes nucleocytoplasmic redistribution in response to B. thetaiotaomicron. A decrease in PPAR-gamma abolishes both the nuclear export of RelA and the anti-inflammatory activity of B. thetaiotaomicron. This PPAR-gamma-dependent anti-inflammatory mechanism defines new cellular targets for therapeutic drug design and interventions for the treatment of chronic inflammation.
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            Intestinal barrier dysfunction in inflammatory bowel diseases.

            Ellen L Simms, Graham Smith, Michael McGuckin … (2008)
            The etiology of human inflammatory bowel diseases (IBDs) is believed to involve inappropriate host responses to the complex commensal microbial flora in the gut, although an altered commensal flora is not completely excluded. A multifunctional cellular and secreted barrier separates the microbial flora from host tissues. Altered function of this barrier remains a major largely unexplored pathway to IBD. Although there is evidence of barrier dysfunction in IBD, it remains unclear whether this is a primary contributor to disease or a consequence of mucosal inflammation. Recent evidence from animal models demonstrating that genetic defects restricted to the epithelium can initiate intestinal inflammation in the presence of normal underlying immunity has refocused attention on epithelial dysfunction in IBD. We review the components of the secreted and cellular barrier, their regulation, including interactions with underlying innate and adaptive immunity, evidence from animal models of the barrier's role in preventing intestinal inflammation, and evidence of barrier dysfunction in both Crohn's disease and ulcerative colitis.
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              Loss of intestinal core 1-derived O-glycans causes spontaneous colitis in mice.

              Jianxin Fu, Bo Wei, Tao Wen … (2011)
              Mucin-type O-linked oligosaccharides (O-glycans) are primary components of the intestinal mucins that form the mucus gel layer overlying the gut epithelium. Impaired expression of intestinal O-glycans has been observed in patients with ulcerative colitis (UC), but its role in the etiology of this disease is unknown. Here, we report that mice with intestinal epithelial cell-specific deficiency of core 1-derived O-glycans, the predominant form of O-glycans, developed spontaneous colitis that resembled human UC, including massive myeloid infiltrates and crypt abscesses. The colitis manifested in these mice was also characterized by TNF-producing myeloid infiltrates in colon mucosa in the absence of lymphocytes, supporting an essential role for myeloid cells in colitis initiation. Furthermore, induced deletion of intestinal core 1-derived O-glycans caused spontaneous colitis in adult mice. These data indicate a causal role for the loss of core 1-derived O-glycans in colitis. Finally, we detected a biosynthetic intermediate typically exposed in the absence of core 1 O-glycan, Tn antigen, in the colon epithelium of a subset of UC patients. Somatic mutations in the X-linked gene that encodes core 1 β1,3-galactosyltransferase-specific chaperone 1 (C1GALT1C1, also known as Cosmc), which is essential for core 1 O-glycosylation, were found in Tn-positive epithelia. These data suggest what we believe to be a new molecular mechanism for the pathogenesis of UC.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Gut Microbes
                Journal ID (iso-abbrev): Gut Microbes
                Journal ID (publisher-id): GMIC
                Title: Gut Microbes
                Publisher: Landes Bioscience
                ISSN (Print): 1949-0976
                ISSN (Electronic): 1949-0984
                Publication date (Print): 01 May 2014
                Publication date (Electronic): 24 March 2014
                Publication date PMC-release: 01 May 2015
                Volume: 5
                Issue: 3
                Pages: 286-295
                Affiliations
                [1 ]Department of Food Science and Technology; University of Nebraska; Lincoln, NE USA
                [2 ]Department of Pathology; Johns Hopkins University School of Medicine; Baltimore, MD USA
                [3 ]Oklahoma Medical Research Foundation; Oklahoma City, OK USA
                [4 ]Junior Research Group Intestinal Microbiome; ZIEL-Research Center for Nutrition and Food Sciences; Technische Universität München; Munich, Germany
                [5 ]Department of Microbiology; Cornell University; Ithaca, NY USA
                Author notes
                [†]

                These authors contributed equally to this work

                [* ]Correspondence to: Lijun Xia, Email: lijun-xia@ 123456omrf.org and Daniel A Peterson, Email: daniel.peterson@ 123456jhmi.edu
                Article
                Publisher ID: 2013GUTMICROBES0119R Publisher Item ID: 28622
                DOI: 10.4161/gmic.28622
                PMC ID: 4153765
                PubMed ID: 24662098
                SO-VID: acd4c22b-4c93-4996-8014-fdeb7839eacd
                Copyright © Copyright © 2014 Landes Bioscience
                License:

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                Date received : 18 December 2013
                Date revision received : 13 March 2014
                Date accepted : 21 March 2014
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: gut microbiota,pyrosequencing,core 1 o-glycans deficient mice,dysbiosis,spontaneous colitis,bacteroides thetaiotaomicron,lactobacillus johnsonii,bacteroides sartorii,clostridium,akkermasia muciniphila
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: gut microbiota, pyrosequencing, core 1 o-glycans deficient mice, dysbiosis, spontaneous colitis, bacteroides thetaiotaomicron, lactobacillus johnsonii, bacteroides sartorii, clostridium, akkermasia muciniphila

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