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

Abstract

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-17mice to confirm the effect of IL-17A on influencing neutrophil attractants expressions. From the analysis of the data, we found that showed that Cm infection could upregulate the expression of neutrophil-related chemokines such as KC, MIP-2 and IL-6, as well as adhesion molecules including ICAM-1 and VCAM-1. With blocking endogenous IL-17A, the upregulated MIP-2 and IL-6 were decreased, which induced less neutrophil recruitment in lung. Comparing to WT mice, IL-17mice showed decreased infiltration of neutrophils in lung during the early phase of Cm infection, which were accordant with decreased chemokines, such as KC, MIP-2 and IL-6 expression. Whereas, the expression of adhesion molecules including ICAM and VCAM-1 in lungs were significantly increased in IL-17mice comparing to WT mice during Cm lung infection. The results demonstrated that IL-17A influenced neutrophil infiltration by affecting expression of chemokines and adhesion molecules during the early phase of chlamydial lung infection.