SYNOVIOCYTE-PACKAGED CHLAMYDIA-TRACHOMATIS INDUCES A CHRONIC ASEPTIC ARTHRITIS

The basic mechanisms underlying reactive arthritis and specifically th e joint injury that follows intra-articular Chlamydia trachomatis infe ction have not been defined. The present study addresses this question through the development of an experimental model. Stable cell lines w ere generated from synoviocytes harvested from the knee joints of Lewi s rats. The synoviocytes were cocultivated with C. trachomatis to allo w invasion by the microbe and were then transferred by intra-articular injection into the knee joints of Lewis rats. The ensuing arthritis c ould be subdivided into an early phase (less than or equal to 14 d) an d a late phase. The early phase was characterized by intense, primaril y neutrophilic, synovitis; accelerated cartilage injury; dissemination of Chlamydia to liver and spleen; and viable Chlamydia in the joints. The late phase was marked by mixed mononuclear lymphocyte infiltratio n in the joint; dysplastic cartilage injury and repair; absence of via ble organisms; and development of a distinctive humoral response. West ern blot analysis comparing reactive arthritis patients to the experim ental model indicates that candidate arthritogenic chlamydial antigens are comparable between the two. This model demonstrates that an inten se synovitis can be induced by this intracellular pathogen, and that c hronic inflammation can persist well beyond the culture-positive phase . Furthermore, these data show that the synoviocyte is a suitable host cell for C. trachomatis and can function as a reservoir of microbial antigens sufficient to perpetuate joint injury.