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      A distinct gut microbiota composition in patients with ankylosing spondylitis is associated with increased levels of fecal calprotectin

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          Abstract

          Background

          Ankylosing spondylitis (AS) shares many characteristics with inflammatory bowel disease (IBD). Intestinal microbiota most likely plays an important role in the development of IBDs and may also be involved in the pathogenesis of AS. We aimed to define and compare the fecal microbiota composition in patients with AS, ulcerative colitis (UC), and healthy controls (HC) and to determine relationships between fecal microbiota, fecal calprotectin, and disease-related variables in AS.

          Methods

          Fecal microbiota composition was assessed with GA-map™ Dysbiosis Test (Genetic Analysis, Oslo, Norway), which also reports the degree of deviation of the microbiota composition compared with a healthy control population, a Dysbiosis Index (DI) score 1–5. The AS patients were assessed with questionnaires, back mobility tests, fecal calprotectin, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).

          Results

          Totally, 150 patients with AS (55% men, median age 55.5 years, median BASDAI 3.2), 18 patients with UC (56% men, median age 30.5 years), and 17 HC (65% men, median age 22 years) were included. Principal component analysis showed highly separate clustering of fecal microbiota from the patients with AS, UC, and HC. Compared with HC, fecal microbiota in AS was characterized by a higher abundance of Proteobacteria, Enterobacteriaceae, Bacilli, Streptococcus species, and Actinobacteria, but lower abundance of Bacteroides and Lachnospiraceae.

          Further, fecal microbiota composition differed between patients with normal (≤ 50 mg/kg, n = 57) and increased (≥ 200 mg/kg, n = 36) fecal calprotectin. Patients with increased fecal calprotectin had lower abundance of bacteria with anti-inflammatory properties such as Faecalibacterium prausnitzii and Clostridium and higher abundance of the genus Streptococcus. No association was found between the fecal microbiota composition and HLAB27 status, disease activity, function, or medication. Dysbiosis (defined as DI ≥ 3) was found in 87% of AS patients.

          Conclusions

          Patients with AS have a distinct fecal microbiota signature, which is linked to fecal calprotectin levels, a marker of intestinal inflammation, but not to other clinical parameters. These findings suggest a local interplay between intestinal microbiota and gut inflammation in AS.

          Trial registration

          ClinicalTrials.gov, NCT00858819. Registered March 9, 2009.

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          Most cited references34

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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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            Roles for Intestinal Bacteria, Viruses, and Fungi in Pathogenesis of Inflammatory Bowel Diseases and Therapeutic Approaches.

            Intestinal microbiota are involved in the pathogenesis of Crohn's disease, ulcerative colitis, and pouchitis. We review the mechanisms by which these gut bacteria, fungi, and viruses mediate mucosal homeostasis via their composite genes (metagenome) and metabolic products (metabolome). We explain how alterations to their profiles and functions under conditions of dysbiosis contribute to inflammation and effector immune responses that mediate inflammatory bowel diseases (IBD) in humans and enterocolitis in mice. It could be possible to engineer the intestinal environment by modifying the microbiota community structure or function to treat patients with IBD-either with individual agents, via dietary management, or as adjuncts to immunosuppressive drugs. We summarize the latest information on therapeutic use of fecal microbial transplantation and propose improved strategies to selectively normalize the dysbiotic microbiome in personalized approaches to treatment.
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              IBD-what role do Proteobacteria play?

              The gastrointestinal microbiota has come to the fore in the search for the causes of IBD. This shift has largely been driven by the finding of genetic polymorphisms involved in gastrointestinal innate immunity (particularly polymorphisms in NOD2 and genes involved in autophagy) and alterations in the composition of the microbiota that might result in inflammation (so-called dysbiosis). Microbial diversity studies have continually demonstrated an expansion of the Proteobacteria phylum in patients with IBD. Individual Proteobacteria, in particular (adherent-invasive) Escherichia coli, Campylobacter concisus and enterohepatic Helicobacter, have all been associated with the pathogenesis of IBD. In this Review, we comprehensively describe the various associations of Proteobacteria and IBD. We also examine the importance of pattern recognition in the extracellular innate immune response of the host with particular reference to Proteobacteria, and postulate that Proteobacteria with adherent and invasive properties might exploit host defenses, drive proinflammatory change, alter the intestinal microbiota in favor of dysbiosis and ultimately lead to the development of IBD.
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                Author and article information

                Contributors
                +46-31-3427745 , eva.klingberg@vgregion.se
                maria.magnusson@microbio.gu.se
                hans.strid@vgregion.se
                anna.deminger@vgregion.se
                arne.stahl@vgregion.se
                johanna.sundin@gu.se
                magnus.simren@medicine.gu.se
                hans.carlsten@rheuma.gu.se
                lena.ohman@microbio.gu.se
                helena.forsblad.delia@umu.se
                Journal
                Arthritis Res Ther
                Arthritis Res. Ther
                Arthritis Research & Therapy
                BioMed Central (London )
                1478-6354
                1478-6362
                27 November 2019
                27 November 2019
                2019
                : 21
                : 248
                Affiliations
                [1 ]ISNI 0000 0000 9919 9582, GRID grid.8761.8, Department of Rheumatology and Inflammation Research, , Sahlgrenska Academy at the University of Gothenburg, ; Gothenburg, Sweden
                [2 ]ISNI 000000009445082X, GRID grid.1649.a, Department of Rheumatology, , Sahlgrenska University Hospital, ; Gröna stråket 14, SE-41345 Gothenburg, Sweden
                [3 ]ISNI 0000 0000 9919 9582, GRID grid.8761.8, Department of Microbiology and Immunology, , Sahlgrenska Academy at the University of Gothenburg, ; Gothenburg, Sweden
                [4 ]ISNI 0000 0004 0624 0304, GRID grid.468026.e, Department of Internal Medicine, , Södra Älvsborgs sjukhus, ; Borås, Sweden
                [5 ]ISNI 0000 0000 9919 9582, GRID grid.8761.8, Department of Internal Medicine and Clinical Nutrition, , Sahlgrenska Academy at the University of Gothenburg, ; Gothenburg, Sweden
                [6 ]ISNI 0000000122483208, GRID grid.10698.36, Center for Functional Gastrointestinal and Motility Disorders, , University of North Carolina at Chapel Hill, ; Chapel Hill, NC USA
                [7 ]ISNI 0000 0001 1034 3451, GRID grid.12650.30, Department of Public Health and Clinical Medicine, Rheumatology, , Umeå University, ; Umeå, Sweden
                Author information
                http://orcid.org/0000-0001-6858-6413
                Article
                2018
                10.1186/s13075-019-2018-4
                6880506
                31771630
                499677d9-86ef-4e25-afd3-db107461b06d
                © The Author(s). 2019

                Open Access This 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
                : 27 March 2019
                : 1 October 2019
                Funding
                Funded by: Swedish state under the agreement between the Swedish Government and the county councils, the ALF-agreement
                Award ID: ALFGBG-64220
                Award Recipient :
                Funded by: The Swedish state under the agreement between the Swedish Government and the county councils, the ALF-agreement
                Award ID: ALFGBG-825511
                Award Recipient :
                Funded by: Västra Götalandsregionen (SE)
                Award ID: VGFOUREG-383071
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100008448, Rune och Ulla Amlövs Stiftelse för Neurologisk och Reumatologisk Forskning;
                Award ID: .
                Award Recipient :
                Funded by: Reumatikerdistriktet i Göteborg (SE)
                Award ID: .
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100005689, Göteborgs Läkaresällskap;
                Award ID: .
                Award Recipient :
                Funded by: COMBINE
                Award ID: .
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100008090, Stiftelsen Reuma Forskningsfond Margareta;
                Award ID: .
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100007687, Svenska Läkaresällskapet;
                Award ID: SLS-409021
                Award Recipient :
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2019

                Orthopedics
                ankylosing spondylitis,spondyloarthritis,microbiota,intestinal inflammation,inflammatory bowel disease

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