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Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder whose precise etiology remains unclear, though growing evidence implicates gut microbiota in its pathogenesis. This study aimed to investigate the role of gut microbiota in the onset and progression of RA by employing fecal microbiota transplantation (FMT) in a collagen-induced arthritis (CIA) mouse model using DBA/1J and Aire−/− strains. Mice received FMT from healthy donors, treatment-naïve RA patients, or treated RA patients in relapse, followed by assessment of microbiota composition via 16S rRNA sequencing, arthritis severity scoring, histological evaluations, and systemic inflammatory markers. The findings revealed distinct microbiota clustering patterns post-FMT across experimental groups, highlighting strain-specific colonization effects. Notably, genera such as Bifidobacterium and Paraprevotella correlated positively with arthritis severity in DBA/1J mice, whereas Corynebacterium, Enterorhabdus, and Odoribacter exhibited negative correlations, suggesting potential protective roles. Despite these microbial differences, minor variations in arthritis scores, paw inflammation, or systemic inflammation were observed among FMT groups. This indicates that although gut microbiota alterations are associated with RA pathogenesis, further investigation with larger cohorts and comprehensive sequencing approaches is essential to elucidate the therapeutic potential of microbiome modulation in autoimmune diseases.

Eosinophilia is uncommon in early rheumatoid arthritis (RA). The most frequent causes of hypereosinophilia during RA treatment are atopic eczema, allergy, helminth infection, haematological malignancy and drug-associated complications. The pathogenesis of this abnormality associated with anti-cytokine therapy is still unknown. We report the case of a young woman with RA and eosinophilia accompanied by systemic symptoms such as dyspnoea, fluid retention and eosinophilic vasculitis. An interesting observation was the persistence of eosinophilia during treatment with various biologics and its normalization after switching to the Janus kinase inhibitor baricitinib.