{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T11:16:17Z","timestamp":1787915777836,"version":"build-2784847793"},"reference-count":161,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T00:00:00Z","timestamp":1787875200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Rheumatoid arthritis (RA) is a chronic, systemic, multifactorial autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction. Although its etiology is complex, accumulating evidence suggests that alterations in the gut microbiota may influence disease susceptibility and progression through interactions with the host immune system. Throughout this review, we discuss the gut microbiota as one component of a broader network of mechanisms contributing to RA pathogenesis rather than as the sole initiating factor. Compromised intestinal barrier integrity and microbial dysbiosis may facilitate the translocation of microbial products, promoting immune activation and loss of tolerance. These alterations have been proposed to contribute to several pathogenic mechanisms, including molecular mimicry, protein citrullination, and disruption of the Th17\/Treg balance, thereby linking mucosal immune responses with synovial inflammation. Patients with RA also frequently exhibit reduced intestinal production of short-chain fatty acids (SCFAs), particularly butyrate, which is associated with decreased abundances of SCFA-producing bacteria, including\n                    <jats:italic>Faecalibacterium<\/jats:italic>\n                    and\n                    <jats:italic>Roseburia<\/jats:italic>\n                    , and lower fecal and circulating butyrate levels. Reduced SCFA availability may further exacerbate inflammatory pathways and impair immune homeostasis. In parallel, gut-imprinted immune cells may migrate to the joints through shared homing pathways, potentially amplifying local inflammation. Taken together, current evidence supports the gut\u2013joint axis as a promising framework for understanding immune dysregulation in RA and highlights microbiota-targeted interventions as potential adjunctive therapeutic strategies.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1884535","type":"journal-article","created":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T10:19:16Z","timestamp":1787912356000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Gut microbiota dysbiosis in rheumatoid arthritis: mechanisms linking intestinal barrier dysfunction to synovial inflammation"],"prefix":"10.3389","volume":"17","author":[{"given":"Shirin","family":"Hafezi","sequence":"first","affiliation":[{"name":"Research Institute for Medical and Health Sciences, University of Sharjah","place":["Sharjah, United Arab Emirates"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fatemeh","family":"Saheb Sharif-Askari","sequence":"additional","affiliation":[{"name":"Research Institute for Medical and Health Sciences, University of Sharjah","place":["Sharjah, United Arab Emirates"]},{"name":"Department of Pharmacy Practice and Pharmacotherapeutics, College of Pharmacy, University of Sharjah","place":["Sharjah, United Arab Emirates"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Narjes","family":"Saheb Sharif-Askari","sequence":"additional","affiliation":[{"name":"Research Institute for Medical and Health Sciences, University of Sharjah","place":["Sharjah, United Arab Emirates"]},{"name":"Department of Clinical Sciences, College of Medicine, University of Sharjah","place":["Sharjah, United Arab Emirates"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariam","family":"Wed Eladham","sequence":"additional","affiliation":[{"name":"Research Institute for Medical and Health Sciences, University of Sharjah","place":["Sharjah, United Arab Emirates"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmed","family":"S. Zayat","sequence":"additional","affiliation":[{"name":"Rheumatology Department, University Hospital Sharjah, University of Sharjah","place":["Sharjah, United Arab Emirates"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rabih","family":"Halwani","sequence":"additional","affiliation":[{"name":"Research Institute for Medical and Health Sciences, University of Sharjah","place":["Sharjah, United Arab Emirates"]},{"name":"Health and Wellbeing Sector, NEOM","place":["Tabuk, Saudi Arabia"]},{"name":"King Saud University Celiac Disease Research Chair, Department of Pediatrics, College of Medicine, King Saud University","place":["Riyadh, Saudi Arabia"]},{"name":"Prince Fahad Bin Sultan Chair for Biomedical Research, University of Tabuk","place":["Tabuk, Saudi Arabia"]},{"name":"College of Medicine, Alfaisal University","place":["Riyadh, Saudi 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