Meta-analysis reveals shared microbial changes in inflammatory bowel disease and autoimmune arthritis, suggesting common etiology.
Objective: Inflammatory bowel disease (IBD) and autoimmune arthritis frequently co-occur and share genetic susceptibility, yet their common gut microbial alterations remain poorly characterized. Methods: We conducted a meta-analysis of two independent 16S rRNA sequencing datasets from the Microbiome HD database, encompassing patients with Crohn’s disease (CD), ulcerative colitis (UC), rheumatoid arthritis (RA) or psoriatic arthritis (PsA). Data were normalized using log-CPM and supervised normalization to remove batch effects. Differential abundance analysis was performed using Wilcoxon tests with FDR correction. A gradient boosting machine (GBM) model was trained to evaluate the diagnostic potential of microbial features. Results: We identified consistent microbial alterations across all four diseases, including significant enrichment of Veillonella and depletion of SCFA-producing genera such as Ethanoligenens, Oscillibacter, Phascolarctobacterium, and Clostridium_IV. The GBM models demonstrated strong diagnostic performance for CD, RA, and PsA (AUC > 0.8), though cross-disease classification performance was variable, indicating both shared and disease-specific microbial features. Conclusion: Our findings reveal a common gut dysbiosis pattern in IBD and arthritis, characterized by the rise of pro-inflammatory taxa and loss of protective bacteria. These shared microbial signatures suggest a potential common etiology involving impaired SCFA metabolism and mucosal immunity, supporting the “gut–joint axis” hypothesis. Microbial biomarkers may serve as diagnostic tools, though disease-specific variations warrant further investigation.
No takes yet. Share an insight, caveat, or question.
Junxian Chen (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: