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      Influence of diet on the gut microbiome and implications for human health

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          Abstract

          Recent studies have suggested that the intestinal microbiome plays an important role in modulating risk of several chronic diseases, including inflammatory bowel disease, obesity, type 2 diabetes, cardiovascular disease, and cancer. At the same time, it is now understood that diet plays a significant role in shaping the microbiome, with experiments showing that dietary alterations can induce large, temporary microbial shifts within 24 h. Given this association, there may be significant therapeutic utility in altering microbial composition through diet. This review systematically evaluates current data regarding the effects of several common dietary components on intestinal microbiota. We show that consumption of particular types of food produces predictable shifts in existing host bacterial genera. Furthermore, the identity of these bacteria affects host immune and metabolic parameters, with broad implications for human health. Familiarity with these associations will be of tremendous use to the practitioner as well as the patient.

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          Most cited references114

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          Short-chain fatty acids and human colonic function: roles of resistant starch and nonstarch polysaccharides.

          Resistant starch (RS) is starch and products of its small intestinal digestion that enter the large bowel. It occurs for various reasons including chemical structure, cooking of food, chemical modification, and food mastication. Human colonic bacteria ferment RS and nonstarch polysaccharides (NSP; major components of dietary fiber) to short-chain fatty acids (SCFA), mainly acetate, propionate, and butyrate. SCFA stimulate colonic blood flow and fluid and electrolyte uptake. Butyrate is a preferred substrate for colonocytes and appears to promote a normal phenotype in these cells. Fermentation of some RS types favors butyrate production. Measurement of colonic fermentation in humans is difficult, and indirect measures (e.g., fecal samples) or animal models have been used. Of the latter, rodents appear to be of limited value, and pigs or dogs are preferable. RS is less effective than NSP in stool bulking, but epidemiological data suggest that it is more protective against colorectal cancer, possibly via butyrate. RS is a prebiotic, but knowledge of its other interactions with the microflora is limited. The contribution of RS to fermentation and colonic physiology seems to be greater than that of NSP. However, the lack of a generally accepted analytical procedure that accommodates the major influences on RS means this is yet to be established.
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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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              Has the microbiota played a critical role in the evolution of the adaptive immune system?

              Although microbes have been classically viewed as pathogens, it is now well established that the majority of host-bacterial interactions are symbiotic. During development and into adulthood, gut bacteria shape the tissues, cells, and molecular profile of our gastrointestinal immune system. This partnership, forged over many millennia of coevolution, is based on a molecular exchange involving bacterial signals that are recognized by host receptors to mediate beneficial outcomes for both microbes and humans. We explore how specific aspects of the adaptive immune system are influenced by intestinal commensal bacteria. Understanding the molecular mechanisms that mediate symbiosis between commensal bacteria and humans may redefine how we view the evolution of adaptive immunity and consequently how we approach the treatment of numerous immunologic disorders.
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                Author and article information

                Contributors
                rasnik.s@gmail.com
                HsinWen.Chang@ucsf.edu
                Di.Yan@ucsf.edu
                kristinamlee24@gmail.com
                ucmakderya@gmail.com
                kirstenw2017@gmail.com
                michaelabrouk1@gmail.com
                bfarahnik@gmail.com
                Mio.Nakamura@ucsf.edu
                tianhao@usc.edu
                Tina.Bhutani@ucsf.edu
                415-476-8364 , wilson.liao@ucsf.edu
                Journal
                J Transl Med
                J Transl Med
                Journal of Translational Medicine
                BioMed Central (London )
                1479-5876
                8 April 2017
                8 April 2017
                2017
                : 15
                : 73
                Affiliations
                [1 ]GRID grid.19006.3e, , University of California, Los Angeles, David Geffen School of Medicine at UCLA, ; Los Angeles, CA 90095 USA
                [2 ]GRID grid.266102.1, Department of Dermatology, , University of California, San Francisco, ; 2340 Sutter St. Room N431, Box 0808, San Francisco, CA 94115 USA
                [3 ]GRID grid.266093.8, , University of California, Irvine, School of Medicine, ; Irvine, CA 92697 USA
                [4 ]GRID grid.59062.38, , University of Vermont College of Medicine, ; Burlington, VT 05405 USA
                [5 ]GRID grid.42505.36, , University of Southern California Keck School of Medicine, ; Los Angeles, CA 90033 USA
                Author information
                http://orcid.org/0000-0001-7883-6439
                Article
                1175
                10.1186/s12967-017-1175-y
                5385025
                28388917
                331d65ee-67dc-4d7a-88ef-c5071e9f8742
                © The Author(s) 2017

                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. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 30 September 2016
                : 21 March 2017
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000069, National Institute of Arthritis and Musculoskeletal and Skin Diseases;
                Award ID: R01AR065174
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000060, National Institute of Allergy and Infectious Diseases;
                Award ID: U01AI119125
                Award Recipient :
                Categories
                Review
                Custom metadata
                © The Author(s) 2017

                Medicine
                diet,health,metabolism,microbiome,microbiota,nutrition
                Medicine
                diet, health, metabolism, microbiome, microbiota, nutrition

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