Conference: American College of Rheumatology Annual Meeting, October 19–24, 2018 Chicago, Illinois, USA.
Conference Highlight: Studies presented support the link between a perturbed gut microbiome, dysbiosis, and spondyloarthritis, including psoriatic arthritis.
Conference Summary: This conference brought together experts to discuss the latest in arthritis research. Dr. Martin Blaser from New York University proposed that gut dysbiosis, or a perturbed microbiota composition, is associated epidemiologically with the rise in autoimmune diseases in the modern era. The microbiome evolves in a dynamic relationship with the host and develops into its adult-like composition by age 3. His theory of Disappearing Microbiota suggests that repeated courses of antibiotics contribute to dysbiosis with metabolic and immunologic effects.
Suggesting an additional mechanism that links dysbiosis and spondyloarthritis (SpA), Eric Norman from the University of Colorado demonstrated intra-epithelial lymphocyte migration from the gut to the spleen and joints in a mouse model of inflammatory bowel disease and SpA that is characterized by gut dysbiosis. The mice also exhibited a decrease in gut and joint inflammation with antibiotic treatment.
Considering the SpA-microbiome link from a clinical standpoint, Dr. Julia Manasson from New York University presented findings on the effect of biologic drugs on the gut microbiome in psoriatic arthritis (PsA) and SpA. The interleukin 17 inhibitor (IL-17i) secukinumab and TNF-alpha inhibitors (TNFi) were associated with distinct changes in several bacterial and fungal taxa pre- vs. post-treatment. For example, Bacteriodales’ relative abundance decreased in most TNFi-treated and increased in a third of IL-17i-treated patients. In addition, IL-17i (but not the TNFi) cohort had high expansion in Candida albicans in 20% of patients. This finding suggests that the microbiome may be implicated in the association of IL-17A monoclonal antibodies with oropharyngeal candidiasis and help identify patients at risk for C. albicans expansion.