Triggers and regulation: the gut microbiome in rheumatoid arthritis

ABSTRACTIntroduction Rheumatoid arthritis is a chronic inflammatory disease marked by systemic symptoms and joint degeneration. Interestingly, the development and progression of rheumatoid arthritis have been linked to the microbiome, notably the gut microbiome. Dysbiosis, an alteration in the gut microbiome, has been connected to the etiology and pathogenesis of rheumatoid arthritis. For instance, dysbiosis increases intestinal permeability and promotes the movement of bacteria and their products, which in turn triggers and aggravates systemic inflammation.Areas covered The correlation between the gut microbiome and RA. Triggers of RA including dysbiosis. The therapeutic potential of the gut microbiome in RA due to its critical function in influencing the immune response. The fecal microbiota transplantation (FMT), a therapeutic strategy that involves the transfer of healthy fecal microbiota from a donor to a recipient, has produced encouraging results in the treatment of several autoimmune illnesses, including rheumatoid arthritis.Expert opinion The role of the gut microbiome in RA is critical and serves as a basis for etiology and pathogenesis, as well as having therapeutic implications. In our opinion, FMT is an excellent example of this correlation. Still, more investigations and well-designed studies are needed in order to make firm conclusions and recommendations.KEYWORDS: Autoimmunityfecal microbial transplantationgut microbiomemicrobiomerheumatoid arthritis Article highlights The etiology and pathogenesis of rheumatoid arthritis is still under active research.The gut microbiome has been investigated in recent decades as a key element in the pathogenesis of rheumatoid arthritis.Alterations in gut microbiome, the 'dysbiosis,' were shown to take place early in the disease.Figuring out and understanding the role of gut microbiome in rheumatoid arthritis have significant implications for the treatment of the disease.Fecal microbiota transplantation has shown beneficial effects in animal models as well as patients with rheumatoid arthritis.Declaration of interestThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.AcknowledgmentsThe authors would like to thank Abdulkarim Alwani (Istanbul Medipol University) for providing the Figure design.Reviewer disclosuresPeer reviewers on this manuscript have no relevant financial or other relationships to disclose.Additional informationFundingThis paper was not funded.