For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
11
views
104
references
 Top references
cited by
51
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      442
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The role of microbiome in rheumatoid arthritis treatment

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Rheumatoid arthritis (RA) is an autoimmune disorder with multifactorial etiology; both genetic and environmental factors are known to be involved in pathogenesis. Treatment with disease-modifying antirheumatic drugs (DMARDs) plays an essential role in controlling disease progression and symptoms. DMARDs have immunomodulatory properties and suppress immune response by interfering in various pro-inflammatory pathways. Recent evidence has shown that the gut microbiota directly and indirectly modulates the host immune system. RA has been associated with dysbiosis of the gut microbiota. Patients with RA treated with DMARDs show partial restoration of eubiotic gut microbiome. Hence, it is essential to understand the impact of DMARDs on the microbial composition and its consequent influences on the host immune system to identify novel therapies for RA. In this review, we discuss the importance of antirheumatic-drug-induced host microbiota modulations and possible probiotics that can generate eubiosis.

          Related collections

          Most cited references104

          • Record: found
          • Abstract: found
          • Article: not found

          Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis.

          Seth Rakoff-Nahoum, Justin Paglino, Fatima Eslami-Varzaneh … (2004)
          Toll-like receptors (TLRs) play a crucial role in host defense against microbial infection. The microbial ligands recognized by TLRs are not unique to pathogens, however, and are produced by both pathogenic and commensal microorganisms. It is thought that an inflammatory response to commensal bacteria is avoided due to sequestration of microflora by surface epithelia. Here, we show that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis. Furthermore, we find that activation of TLRs by commensal microflora is critical for the protection against gut injury and associated mortality. These findings reveal a novel function of TLRs-control of intestinal epithelial homeostasis and protection from injury-and provide a new perspective on the evolution of host-microbial interactions.
          Article 0 comments Cited 1103 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            An immunomodulatory molecule of symbiotic bacteria directs maturation of the host immune system.

            Sarkis Mazmanian, Cui Hua Liu, Arthur O Tzianabos … (2005)
            The mammalian gastrointestinal tract harbors a complex ecosystem consisting of countless bacteria in homeostasis with the host immune system. Shaped by evolution, this partnership has potential for symbiotic benefit. However, the identities of bacterial molecules mediating symbiosis remain undefined. Here we show that, during colonization of animals with the ubiquitous gut microorganism Bacteroides fragilis, a bacterial polysaccharide (PSA) directs the cellular and physical maturation of the developing immune system. Comparison with germ-free animals reveals that the immunomodulatory activities of PSA during B. fragilis colonization include correcting systemic T cell deficiencies and T(H)1/T(H)2 imbalances and directing lymphoid organogenesis. A PSA mutant of B. fragilis does not restore these immunologic functions. PSA presented by intestinal dendritic cells activates CD4+ T cells and elicits appropriate cytokine production. These findings provide a molecular basis for host-bacterial symbiosis and reveal the archetypal molecule of commensal bacteria that mediates development of the host immune system.
            Article 0 comments Cited 949 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells.

              Hsin-Jung J. Wu, Ivaylo Ivanov, Jaime Darce … (2010)
              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.
              Article 0 comments Cited 555 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Rahul Bodkhe
                Baskar Balakrishnan
                Veena Taneja:
                ORCID: https://orcid.org/0000-0003-2401-694X
                Journal
                Journal ID (nlm-ta): Ther Adv Musculoskelet Dis
                Journal ID (iso-abbrev): Ther Adv Musculoskelet Dis
                Journal ID (publisher-id): TAB
                Journal ID (hwp): sptab
                Title: Therapeutic Advances in Musculoskeletal Disease
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Print): 1759-720X
                ISSN (Electronic): 1759-7218
                Publication date (Electronic): 30 July 2019
                Publication date Collection: 2019
                Volume: 11
                Electronic Location Identifier: 1759720X19844632
                Affiliations
                [1-1759720X19844632]Department of Immunology, Mayo Clinic, Rochester, MN, USA
                [2-1759720X19844632]Department of Immunology, Mayo Clinic, Rochester, MN, USA
                [3-1759720X19844632]Department of Immunology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
                Author notes
                Author information
                https://orcid.org/0000-0003-2401-694X
                Article
                Publisher ID: 10.1177_1759720X19844632
                DOI: 10.1177/1759720X19844632
                PMC ID: 6685117
                PubMed ID: 31431810
                SO-VID: d5c842f0-b865-408a-9c84-208553222c66
                Copyright © © The Author(s), 2019
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 1 February 2019
                Date accepted : 25 March 2019
                Funding
                Funded by: U.S. Department of Defense, FundRef https://doi.org/10.13039/100000005;
                Award ID: W81XWH-15-1-0213
                Funded by: mayo foundation for medical education and research, FundRef https://doi.org/10.13039/100007048;
                Categories
                Subject: Review
                Custom metadata
                cover-date January-December 2019

                Keywords: disease-modifying antirheumatic drugs,gut microbiota,immune modulation,microbial modulation,probiotics,rheumatoid arthritis
                Data availability:
                Keywords: disease-modifying antirheumatic drugs, gut microbiota, immune modulation, microbial modulation, probiotics, rheumatoid arthritis

                Comments

                Comment on this article

                scite_

                Similar content442

                See all similar

                Cited by51

                See all cited by

                Most referenced authors2,914

                See all reference authors