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.