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Specific taxa - including Prevotella copri, Collinsella aerofaciens, and reductions in butyrate-producing bacteria - have been linked to heightened systemic inflammation, increased T helper 17 responses, and the generation of RA-associated autoantibodies. Current research also indicates that anti-rheumatic medications such as methotrexate, sulfasalazine, and minocycline produce measurable shifts in gut microbial composition, suggesting that microbiota-drug interactions may influence treatment response. Therapeutic approaches aimed at modifying gut ecology - including dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation - show early potential in restoring microbial balance, improving intestinal barrier integrity, and reducing inflammatory markers, although evidence in the preclinical RA stage remains limited. Additionally, emerging data highlight the importance of intestinal autophagy and microRNA networks in regulating epithelial integrity and systemic immune activation. Taken together, the literature supports a mechanistic link between gut dysbiosis and the onset of RA. It points to microbiota-targeted strategies as promising avenues for delaying or preventing disease progression. 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