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      Characterization of the fecal microbiome in cats with inflammatory bowel disease or alimentary small cell lymphoma

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          Abstract

          Feline chronic enteropathy (CE) is a common gastrointestinal disorder in cats and mainly comprises inflammatory bowel disease (IBD) and small cell lymphoma (SCL). Both IBD and SCL in cats share features with chronic enteropathies such as IBD and monomorphic epitheliotropic intestinal T-cell lymphoma in humans. The aim of this study was to characterize the fecal microbiome of 38 healthy cats and 27 cats with CE (13 cats with IBD and 14 cats with SCL). Alpha diversity indices were significantly decreased in cats with CE (OTU p = 0.003, Shannon Index p = 0.008, Phylogenetic Diversity p = 0.019). ANOSIM showed a significant difference in bacterial communities, albeit with a small effect size ( P = 0.023, R = 0.073). Univariate analysis and LEfSE showed a lower abundance of facultative anaerobic taxa of the phyla Firmicutes (families Ruminococcaceae and Turicibacteraceae), Actinobacteria (genus Bifidobacterium) and Bacteroidetes (i.a. Bacteroides plebeius) in cats with CE. The facultative anaerobic taxa Enterobacteriaceae and Streptococcaceae were increased in cats with CE. No significant difference between the microbiome of cats with IBD and those with SCL was found. Cats with CE showed patterns of dysbiosis similar to those in found people with IBD.

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          Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing

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            Potential beneficial effects of butyrate in intestinal and extraintestinal diseases

            The multiple beneficial effects on human health of the short-chain fatty acid butyrate, synthesized from non-absorbed carbohydrate by colonic microbiota, are well documented. At the intestinal level, butyrate plays a regulatory role on the transepithelial fluid transport, ameliorates mucosal inflammation and oxidative status, reinforces the epithelial defense barrier, and modulates visceral sensitivity and intestinal motility. In addition, a growing number of studies have stressed the role of butyrate in the prevention and inhibition of colorectal cancer. At the extraintestinal level, butyrate exerts potentially useful effects on many conditions, including hemoglobinopathies, genetic metabolic diseases, hypercholesterolemia, insulin resistance, and ischemic stroke. The mechanisms of action of butyrate are different; many of these are related to its potent regulatory effects on gene expression. These data suggest a wide spectrum of positive effects exerted by butyrate, with a high potential for a therapeutic use in human medicine.
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              Butyrate inhibits inflammatory responses through NFkappaB inhibition: implications for Crohn's disease.

              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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                Author and article information

                Contributors
                SMarsilio@ucdavis.edu
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                16 December 2019
                16 December 2019
                2019
                : 9
                : 19208
                Affiliations
                [1 ]ISNI 0000 0004 4687 2082, GRID grid.264756.4, Gastrointestinal Laboratory, Department of Small Animal Clinical Science, , Texas A&M University, 4474 TAMU, ; College Station, TX 77843-4474 USA
                [2 ]ISNI 0000 0004 1936 9684, GRID grid.27860.3b, University of California Davis, School of Veterinary Medicine, Department of Medicine & Epidemiology, ; Davis, CA 95616 USA
                [3 ]Veterinary Specialty Hospital, 10435 Sorrento Valley Rd, San Diego, CA 92121 USA
                [4 ]ISNI 0000 0001 2112 1969, GRID grid.4391.f, Oregon Veterinary Diagnostic Laboratory, Carlson College of Veterinary Medicine, , Oregon State University, ; Corvallis, OR USA
                [5 ]Texas Veterinary Pathology, LLC, San Antonio, TX USA
                [6 ]Present Address: VCA Animal Specialty & Emergency Center, 1535 South Sepulveda Blvd, Los Angeles, CA 90025 USA
                [7 ]Present Address: Flagstaff Veterinary Internal Medicine Consulting (FLG VIM-C), 6135 Kaitlin Way, Flagstaff, AZ 86003 USA
                Author information
                http://orcid.org/0000-0002-7775-3719
                Article
                55691
                10.1038/s41598-019-55691-w
                6914782
                31844119
                c2e01f19-cdff-424a-a41f-3e348193c8c9
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 7 January 2019
                : 30 November 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/100003516, Winn Feline Foundation (WFF);
                Award ID: MT16-018
                Award Recipient :
                Categories
                Article
                Custom metadata
                © The Author(s) 2019

                Uncategorized
                microbiome,dysbiosis
                Uncategorized
                microbiome, dysbiosis

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