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      Immunomodulating Activity and Therapeutic Effects of Short Chain Fatty Acids and Tryptophan Post-biotics in Inflammatory Bowel Disease

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          Crohn's disease (CD) and Ulcerative colitis (UC) are grouped as Inflammatory Bowel Diseases (IBD). The IBD is associated to a multifaceted interplay between immunologic, microbial, genetic, and environmental factors. Nowadays, the gut microbiota (GM) dysbiosis has been indicated as a cause in the IBD development, affecting the impaired cross-talk between GM and immune cells. Moreover, recent studies have uncovered a crucial role for bacterial post-biotics (metabolites) in the orchestration of the host immune response, as they could be messengers between the GM and the immune system. In addition, transgenic mouse models showed that SCFAs (Short Chain Fatty Acids) and Tryptophan (Trp) post-biotics play important immunomodulatory effects, regulating both innate and adaptive immune cell generation, their function and trafficking. Here, we present an overview on the main microbial post-biotics and their effects on the gut mucosa with specific emphasis on their relevance for IBD. Finally, we discuss the therapeutic potential of SCFA and Trp post-biotics on IBD through approaches based on the “immunonutrition,” defined as a modulation of the immune system provided by specific interventions that modify dietary nutrients.

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          Most cited references 55

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          The microbiome in inflammatory bowel disease: current status and the future ahead.

          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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            Butyrate inhibits inflammatory responses through NFkappaB inhibition: implications for Crohn's disease.

             J.-P. Segain (2000)
            Proinflammatory cytokines are key factors in the pathogenesis of Crohn's disease (CD). Activation of nuclear factor kappa B (NFkappaB), which is involved in their gene transcription, is increased in the intestinal mucosa of CD patients. As butyrate enemas may be beneficial in treating colonic inflammation, we investigated if butyrate promotes this effect by acting on proinflammatory cytokine expression. Intestinal biopsy specimens, isolated lamina propria cells (LPMC), and peripheral blood mononuclear cells (PBMC) were cultured with or without butyrate for assessment of secretion of tumour necrosis factor (TNF) and mRNA levels. NFkappaB p65 activation was determined by immunofluorescence and gene reporter experiments. Levels of NFkappaB inhibitory protein (IkappaBalpha) were analysed by western blotting. The in vivo efficacy of butyrate was assessed in rats with trinitrobenzene sulphonic acid (TNBS) induced colitis. Butyrate decreased TNF production and proinflammatory cytokine mRNA expression by intestinal biopsies and LPMC from CD patients. Butyrate abolished lipopolysaccharide (LPS) induced expression of cytokines by PBMC and transmigration of NFkappaB from the cytoplasm to the nucleus. LPS induced NFkappaB transcriptional activity was decreased by butyrate while IkappaBalpha levels were stable. Butyrate treatment also improved TNBS induced colitis. Butyrate decreases proinflammatory cytokine expression via inhibition of NFkappaB activation and IkappaBalpha degradation. These anti-inflammatory properties provide a rationale for assessing butyrate in the treatment of CD.
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              A primitive T cell-independent mechanism of intestinal mucosal IgA responses to commensal bacteria.

              The immunoglobulin A (IgA) is produced to defend mucosal surfaces from environmental organisms, but host defenses against the very heavy load of intestinal commensal microorganisms are poorly understood. The IgA against intestinal commensal bacterial antigens was analyzed; it was not simply "natural antibody" but was specifically induced and responded to antigenic changes within an established gut flora. In contrast to IgA responses against exotoxins, a significant proportion of this specific anti-commensal IgA induction was through a pathway that was independent of T cell help and of follicular lymphoid tissue organization, which may reflect an evolutionarily primitive form of specific immune defense.

                Author and article information

                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                22 November 2019
                : 10
                1Department of Clinical and Experimental Medicine, University of Florence , Florence, Italy
                2Department of Health Professions, Dietary Production Line and Nutrition, Azienda Ospedaliera Universitaria Careggi , Florence, Italy
                3SOD of Interdisciplinary Internal Medicine, Azienda Ospedaliera Universitaria Careggi , Florence, Italy
                Author notes

                Edited by: Nuno Empadinhas, University of Coimbra, Portugal

                Reviewed by: Ian Antheni Myles, National Institutes of Health (NIH), United States; Yaqing Qie, University of Texas MD Anderson Cancer Center, United States

                *Correspondence: Amedeo Amedei amedeo.amedei@ 123456unifi.it

                This article was submitted to Nutritional Immunology, a section of the journal Frontiers in Immunology

                Copyright © 2019 Russo, Giudici, Fiorindi, Ficari, Scaringi and Amedei.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 114, Pages: 10, Words: 8666
                Funded by: Ente Cassa di Risparmio di Firenze 10.13039/501100003056


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