Immunopathogenesis of reactive arthritis: role of the cytokines

Abstract

Reactive arthritis (ReA), also known as postinfectious arthritis, belongs to the group of related arthropathies known as spondyloarthritis (SpA). ReA can arise 1-4 weeks 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.