Published online Jul 27, 2014. doi: 10.5411/wji.v4.i2.78
Revised: May 24, 2014
Accepted: June 14, 2014
Published online: July 27, 2014
Reactive arthritis (ReA), also known as sterile postinfectious arthritis, belongs to the group of related arthropathies known as spondyloarthritis (SpA). ReA can arise 1-4 wk after a gastrointestinal or genitourinary infection, but once arthritis develops, the microorganism is not found in the joint. The classical microbes associated with ReA development include Gram-negative aerobic or microaerophilic bacteria containing LPS in their outer membrane. The immunopathogenic mechanisms involved in ReA development are still unknown. A hypothesis suggested that the bacteria probably persist outside the joint, at sites such as gut mucosa or lymph nodes, and bacterial antigens might then be transported to the joints. On the other hand, an altered immune response and the unbalanced production of cytokines have been reported in subjects with ReA. Currently, there is increased evidence to suggest that both mechanisms would operate in the immunopathogenesis of ReA. In this review we highlight recent advances on the role of cytokines in the ReA. Particularly, we discuss the roles of some pro- and anti-inflammatory cytokines involved in the immunopathogenesis of ReA.
Core tip: The immunopathogenic mechanisms involved in reactive arthritis (ReA) development are still unknown. However, in the last years, increased evidence suggests that the immune response in particular certain cytokines could be involved in the pathogenesis of ReA. Currently, the use of biological agents that block the action of certain cytokines has contributed to improving the treatment of some rheumatic pathology. Understanding the role of cytokines in the pathogenesis of ReA could contribute to the development of future treatments. In this review, we highlight recent advances on the role of certain cytokines in the pathogenesis of ReA.