Abstract
The links between the bowel and spondyloarthritis, although demonstrated many years ago, have been placed under the spotlight by recent findings. Thus, studies have established that bowel inflammation is associated with the joint disease activity, sacroiliac joint inflammation by magnetic resonance imaging, and elevated levels of biomarkers for bowel inflammation (S100 proteins) or antimicrobial antibodies (anti-flagellin). IL-23/Th17 pathway activation originating in the bowel has been documented in studies demonstrating that lymphoid cells expressing the IL-23 receptor can migrate to the bloodstream, bone marrow, and joints, via a mechanism involving adhesion molecules. Bacteria present in the bowel are increasingly emerging as major players. Thus, dysbiosis of the bowel microbiota can induce IL-23 production and local inflammatory responses. These new data suggest avenues of research for future treatments.
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