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      Manipulating resident microbiota to enhance regulatory immune function to treat inflammatory bowel diseases

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          Abstract

          Altered intestinal microbial composition (dysbiosis) and metabolic products activate aggressive mucosal immune responses that mediate inflammatory bowel diseases (IBD). This dysbiosis impairs the function of regulatory immune cells, which normally promote mucosal homeostasis. Normalizing and maintaining regulatory immune cell function by correcting dysbiosis provides a promising approach to treat IBD patients. However, existing microbe-targeted therapies, including antibiotics, prebiotics, probiotics, and fecal microbial transplantation, provide variable outcomes that are not optimal for current clinical application. This review discusses recent progress in understanding the dysbiosis of IBD and the basis for therapeutic restoration of homeostatic immune function by manipulating an individual patient’s microbiota composition and function. We believe that identifying more precise therapeutic targets and developing appropriate rapid diagnostic tools will guide more effective and safer microbe-based induction and maintenance treatments for IBD patients that can be applied in a personalized manner.

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          Formation of propionate and butyrate by the human colonic microbiota

          Petra Louis, Harry J. Flint (2017)
          The human gut microbiota ferments dietary non-digestible carbohydrates into short-chain fatty acids (SCFA). These microbial products are utilized by the host and propionate and butyrate in particular exert a range of health-promoting functions. Here an overview of the metabolic pathways utilized by gut microbes to produce these two SCFA from dietary carbohydrates and from amino acids resulting from protein breakdown is provided. This overview emphasizes the important role played by cross-feeding of intermediary metabolites (in particular lactate, succinate and 1,2-propanediol) between different gut bacteria. The ecophysiology, including growth requirements and responses to environmental factors, of major propionate and butyrate producing bacteria are discussed in relation to dietary modulation of these metabolites. A detailed understanding of SCFA metabolism by the gut microbiota is necessary to underpin effective strategies to optimize SCFA supply to the host.
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            The microbiome in inflammatory bowel disease: current status and the future ahead.

            Aleksandar D. Kostic, Ramnik Xavier, Dirk Gevers (2014)
            Studies of the roles of microbial communities in the development of inflammatory bowel disease (IBD) have reached an important milestone. A decade of genome-wide association studies and other genetic analyses have linked IBD with loci that implicate an aberrant immune response to the intestinal microbiota. More recently, profiling studies of the intestinal microbiome have associated the pathogenesis of IBD with characteristic shifts in the composition of the intestinal microbiota, reinforcing the view that IBD results from altered interactions between intestinal microbes and the mucosal immune system. Enhanced technologies can increase our understanding of the interactions between the host and its resident microbiota and their respective roles in IBD from both a large-scale pathway view and at the metabolic level. We review important microbiome studies of patients with IBD and describe what we have learned about the mechanisms of intestinal microbiota dysfunction. We describe the recent progress in microbiome research from exploratory 16S-based studies, reporting associations of specific organisms with a disease, to more recent studies that have taken a more nuanced view, addressing the function of the microbiota by metagenomic and metabolomic methods. Finally, we propose study designs and methodologies for future investigations of the microbiome in patients with inflammatory gut and autoimmune diseases in general. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
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              The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota.

              June Round, S Lee, Jennifer Li … (2011)
              Mucosal surfaces constantly encounter microbes. Toll-like receptors (TLRs) mediate recognition of microbial patterns to eliminate pathogens. By contrast, we demonstrate that the prominent gut commensal Bacteroides fragilis activates the TLR pathway to establish host-microbial symbiosis. TLR2 on CD4(+) T cells is required for B. fragilis colonization of a unique mucosal niche in mice during homeostasis. A symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) regulatory T cells to promote immunologic tolerance. B. fragilis lacking PSA is unable to restrain T helper 17 cell responses and is defective in niche-specific mucosal colonization. Therefore, commensal bacteria exploit the TLR pathway to actively suppress immunity. We propose that the immune system can discriminate between pathogens and the microbiota through recognition of symbiotic bacterial molecules in a process that engenders commensal colonization.
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                Author and article information

                Contributors
                Ryan Balfour Sartor: rbs@med.unc.edu
                Journal
                Journal ID (nlm-ta): J Gastroenterol
                Journal ID (iso-abbrev): J. Gastroenterol
                Title: Journal of Gastroenterology
                Publisher: Springer Japan (Tokyo )
                ISSN (Print): 0944-1174
                ISSN (Electronic): 1435-5922
                Publication date (Electronic): 3 September 2019
                Publication date PMC-release: 3 September 2019
                Publication date (Print): 2020
                Volume: 55
                Issue: 1
                Pages: 4-14
                Affiliations
                [1 ]GRID grid.411621.1, ISNI 0000 0000 8661 1590, Department of Internal Medicine II, Faculty of Medicine, , Shimane University, ; Izumo, Shimane Japan
                [2 ]GRID grid.410711.2, ISNI 0000 0001 1034 1720, Center for Gastrointestinal Biology and Disease, Division of Gastroenterology and Hepatology, Department of Medicine, , University of North Carolina, ; Room 7309A MBRB, CB# 7032, Chapel Hill, NC 27599-7032 USA
                Article
                Publisher ID: 1618
                DOI: 10.1007/s00535-019-01618-1
                PMC ID: 6942586
                PubMed ID: 31482438
                SO-VID: f52f5d5d-1b99-48ff-a541-dec317bc0e0b
                Copyright © © The Author(s) 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 9 August 2019
                Date accepted : 20 August 2019
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Japanese Society of Gastroenterology 2020

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: crohn’s disease,ulcerative colitis,treatment,bacteria,live biotherapeutic products
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: crohn’s disease, ulcerative colitis, treatment, bacteria, live biotherapeutic products

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