The Stool and Oral Microbiome of Rheumatoid Arthritis Patients Taking Disease‐Modifying Antirheumatic Drugs

Objective: Rheumatoid arthritis (RA) is a common musculoskeletal condition with an estimated prevalence of 0.27% in Australia and New Zealand. Recently, interest in the role of the human microbiome regarding RA pathogenesis has increased. This study is aimed at determining the composition of the stool and oral microbiome of RA patients taking common disease‐modifying antirheumatic drugs (DMARDs). Methods: For this cross‐sectional study, RA patients ( n = 28) with established disease (> 12 months since diagnosis) and healthy individuals ( n = 10) were recruited by the Australian Arthritis and Autoimmune Biobank Collaborative (A3BC). Stool samples and oral swabs were collected, processed, and sequenced to obtain 16s rRNA amplicon sequencing data. Data was processed using a QIIME2/DADA2 pipeline. Diversity and taxonomic analyses were performed using QIIME2 core metrics functions and RStudio packages. Results: Diversity analyses identified differences in the RA stool microbiome, in comparison to healthy controls and between RA patients taking different DMARDs. This includes differences in microbial richness, diversity, and structure. For example, the microbiome of patients taking JAK inhibitors (JAKis) significantly differed to the microbiome of patients on combination therapy (TNF inhibitors [TNFi] +/− methotrexate [MTX]) or taking MTX only. Furthermore, patients taking MTX had a more similar microbiome to healthy individuals. In contrast, limited differences in the oral microbiome were observed for all diversity metrics, although a number of taxa previously linked to oral disease were identified as differentially abundant to healthy individuals. Conclusion: Differences in the diversity and taxa of the stool and oral microbiome of patients with established RA were identified. Overall, there was some concordance with previous research. This work highlights the importance of further investigation into the impact of JAKi, TNFi, and MTX on the RA microbiome.