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- W62488085 abstract "The type III secretion (T3S) apparatus is a virulence factor in many gram negative bacteria such as Pseudomonas spp., Salmonella spp., and Chlamydia spp. Depending on the bacterial species, T3S has been shown to initiate inflammation or inhibit cytokine production. The goal of the present study was to determine how the chlamydial T3S apparatus modulates the host inflammatory response. Since there is no genetic system for Chlamydia spp., blockade of T3S was accomplished pharmacologically. Infections of murine peritoneal macrophages were performed using the mouse biovar Chlamydia muridarum, in an ex vivo infection model. These infections were carried out in the presence or absence of the T3S inhibitor. The resulting expression of the proinflammatory cytokines Tumor Necrosis Factor (TNF)-alpha, Interleukin (IL)-1beta, and IL-6 and the chemokine CXCL-10 were monitored experimentally by quantitative RT-PCR and Enzyme Linked Immunosorbent Assays. Overall, T3S inhibition led to decreased IL-6, IL-1beta, and CXCL-10 production and inhibited bacterial growth at 24 hours post infection while TNF-alpha levels were unaffected. Concomitant addition of exogenous iron sulfate restored growth but not cytokine production, suggesting this latter impairment was dependent on T3S and not growth. This study was supported by NIH grant #AI067678." @default.
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- W62488085 date "2008-04-01" @default.
- W62488085 modified "2023-10-16" @default.
- W62488085 title "The role of the chlamydial Type III secretion apparatus on host cytokine expression" @default.
- W62488085 doi "https://doi.org/10.1096/fasebj.22.2_supplement.549" @default.
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