A clear etiological link has been established between infection with several gram-negative enteric pathogens, including Salmonella spp., and the incidence of reactive arthritis (ReA), an autoimmune disease that largely affects the joints. ReA is sometimes referred to as Reiter's syndrome, particularly when accompanied by uveitis and urethritis. This review reviews the evidence etiologically linking Salmonella infection with autoimmune disease and addresses the roles that bacterial and host elements play in controlling disease outcome. ReA is an autoimmune disease that largely consists of painful joint inflammation but also can include inflammation of the eye, gastrointestinal tract, and skin. ReA is a member of a broad spectrum of chronic inflammatory disorders termed the seronegative spondyloarthropathies (SNSpAs) that includes ankylosing spondylitis (AS), psoriatic arthritis, and enteropathic arthritis. Salmonella species, as well as other enteric pathogens associated with postgastroenteritis ReA, are facultative intracellular gram-negative bacteria. Many studies have analyzed the association of the HLA class I molecule, HLA-B27, with SNSpAs. Whereas B27 has been shown to be present in 90 to 95% of cases of AS, the association of the B27 haplotype with other SNSpAs is more tenuous. The clear association between ReA and infection with Salmonella or other gram-negative enteric pathogens has led to the suggestion that the adaptive immune response to infection has an autoimmune component. In addition to various Salmonella species, other gram-negative enteric pathogens have been linked to the development of ReA. Given their close relationship to Salmonella, this review considers the involvement of Shigella species in ReA.
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