trachomatis has been seldom reported, and thus the organism might not be sought by clinicians. While sexually acquired reactive arthritis is well recognized following urogenital Chlamydia trachomatis infections, the association with rectal infection by LGV-associated serovars of C. We describe 3 cases of sexually acquired reactive arthritis following rectal lymphogranuloma venereum (LGV) infection in London men who have sex with men. Three cases of reactive arthritis secondary to lymphogranuloma venereum. We describe, for the first time to our knowledge, a case of a Chlamydia trachomatis-related reactive arthritis refractory to methotrexate and sulphasalazine that was successfully treated with the monoclonal antibody anti-TNF-alpha and infliximab. Most of the cases are self-limited, lasting some weeks to months, and respond well to nonsteroidal anti-inflammatory drugs (NSAIDs), but a considerable number of cases (about 20%) run a chronic disabling course, requiring immunosuppressants (methotrexate, sulphasalazine) to adequate control of the inflammatory symptoms. Reactive arthritis is an autoimmune disease that develops 2-4 weeks after a triggering infection, resulting mainly in synovitis/enthesitis of the lower limbs, but with a wide array of possible extra-articular manifestations. Infliximab for reactive arthritis secondary to Chlamydia trachomatis infection. trachomatis and can function as a reservoir of microbial antigens sufficient to perpetuate joint injury. Furthermore, these data show that the synoviocyte is a suitable host cell for C. This model demonstrates that an intense synovitis can be induced by this intracellular pathogen, and that chronic inflammation can persist well beyond the culture-positive phase. Western blot analysis comparing reactive arthritis patients to the experimental model indicates that candidate arthritogenic chlamydial antigens are comparable between the two. The late phase was marked by mixed mononuclear lymphocyte infiltration in the joint dysplastic cartilage injury and repair absence of viable organisms and development of a distinctive humoral response. The ensuing arthritis could be subdivided into an early phase (Chlamydia to liver and spleen and viable Chlamydia in the joints. trachomatis to allow invasion by the microbe and were then transferred by intra-articular injection into the knee joints of Lewis rats. The synoviocytes were cocultivated with C. Stable cell lines were generated from synoviocytes harvested from the knee joints of Lewis rats. The present study addresses this question through the development of an experimental model. The basic mechanisms underlying reactive arthritis and specifically the joint injury that follows intra-articular Chlamydia trachomatis infection have not been defined. Synoviocyte-packaged Chlamydia trachomatis induces a chronic aseptic arthritis.
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