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Following a <i>Chlamydia trachomatis</i> infection, the host immune response is characterized by its recognition via Toll-like and Nod-like Receptors, and the subsequent activation of interferon (IFN)-γ-mediated signaling pathways. Recently, the inflammasome-mediated host cell response has emerged to play a role in the physiopathology of <i>C. trachomatis</i> infection. Here we investigated, for the first time, the interaction of IFN-γ and inflammasome in an in vitro model of <i>C. trachomatis</i>-infected primary human synovial cells. Chlamydial replication as well as the expression of caspase-1, IL-1β, as well as IL-18 and IL-6, were assayed. Our results demonstrated the inhibitory activity of IFN-γ by interfering with the inflammasome network through the downregulation of caspase-1 mRNA expression. In addition, the ability of <i>C. trachomatis</i> to hinder the inflammasome pathway favoring its intracellular survival within synovial cells, was observed. Overall, our data suggest a potential mechanism of immune evasion by <i>C. trachomatis</i> in synovial cells, that may be contested by IFN-γ.