Endogenous IL-17A mediated neutrophil infiltration by promoting chemokines expression during chlamydial lung infection.

Chlamydia is an obligate intracellular bacteria, which can infect cervix, urethra, conjunctiva, joints, lungs and so on. Neutrophils are important in host protection against microbial invasion during the early phase of infection. Here, to investigate the mechanism of IL-17A in recruiting neutrophils during Chlamydia muridarum (Cm) lung infection, we introduced IL-17A antibodies and IL-17 mice to confirm the effect of IL-17A on influencing neutrophil attractants expressions.

V4+ T Cells: A Novel IL-17-Producing T Subsets during the Early Phase of Chlamydial Airway Infection in Mice.

Our previous studies showed that T cells provided immune protection against Chlamydial (Cm), an obligate intracellular strain of chlamydia trachomatis, lung infection by producing abundant IL-17. In this study, we investigated the proliferation and activation of lung T cell subsets, specifically the IL-17 and IFN production by them following Cm lung infection. Our results found that five T cell subsets, V1+ T, V2+ T, V4+ T, V5+ T, and V6+ T, expressed in lungs of naïve mice, while Cm lung infection mainly induced the proliferation and activation of V4+ T cells at day 3 p.