Exploring the pathogenesis of RA through the gut-articular axis-dysbiosis a potential factor.

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease with a complex etiology. It has been suggested that the pathogenesis of RA begins in the mucosa and then transitions to the joints when many factors interact, including microbial dysbiosis, inflammatory responses, and immune abnormalities at the mucosal site. Data from RA animals and patients suggest there are changes in the mucosal microflora before the onset of RA, and that dysbiosis of the mucosal ecology continues to play a role in the development of arthritis. Microbial dysbiosis of the mucosa reduces the normal barrier function of the intestinal tract, promotes inflammatory reactions in the mucosal areas of the intestines, and then activates the intestinal immune cells abnormally to produce a large number of auto-reactive antibodies that exacerbate arthritis. Current findings do not clarify whether dysbiosis is only a potential trigger for the development of RA. If it is possible to intervene in such microbial changes before the onset of RA, could the clinical symptoms of arthritis be prevented or reduced? Finding new ways to regulate gut flora composition to maintain gut barrier function is an ongoing challenge for the prevention and treatment of RA.