The role of the gut and intestinal dysbiosis in the pathogenesis of spondyloarthritis

Abstract

Spondyloarthritis (SpA) encompasses chronic inflammatory diseases affecting both axial and peripheral joints. Emerging evidence highlights a pivotal role for the gut–joint axis in SpA pathogenesis, where intestinal dysbiosis and barrier dysfunction facilitate microbial translocation and trigger systemic immune activation. Clinical observations of subclinical gut inflammation, alongside findings from HLA-B27 transgenic rats and SKG mice, underscore the gut's role in initiating joint pathology. Genetic predispositions, particularly HLA-B27, further exacerbate these processes through mechanisms such as endoplasmic reticulum stress and IL-23-mediated T-cell activation. This review integrates epidemiological, mechanistic, and experimental insights to elucidate the complex interplay between the gut microbiota and immune responses in SpA, outlining potential avenues for targeted intervention.