γδT cells promoted the Th17 immune responses in mice with Chlamydia muridarum lung infection

Abstract

Objective To investigate the functions of γδT cells in a mouse model of Chlamydia muridarum (Cm) lung infection and their effects on Chlamydia-specific immunity. Methods Wild type (WT) and TCRδ-/- mice were infected with 1×103 inclusion forming units (IFU) of Cm by nasal inhalation to establish the murine model of Chlamydia respiratory infection. The bodyweight of each mouse was monitored daily. The growth of Chlamydia strains in lung tissues was measured by using enzyme immunoassay (EIA) and represented by IFU. ELISA was used to measure the levels of IFN-γ and IL-17 in the supernatants of spleen cell culture. The levels of IFN-γ and IL-17 secreted by CD3+ CD4+ T cells were determined by using the intracellular cytokine staining assay for evaluating the roles and mechanisms of γδT cells in regulating the Th1 and Th17 immune responses to Chlamydia strains. Results The murine model of Chlamydia pneumonitis was established by nasal inhalation of Cm strains. Compared with the WT mice, the TCR-/- mice showed a significant decrease in bodyweight after Cm infection. No significant difference in the growth of Chlamydia strains in lung tissues was observed between mice from the two groups. Results of the ELISA showed that the levels of IFN-γ in the supernatants of spleen cell culture from WT mice group were similar to those form TCRδ-/- mice groups on days 3 and 7 after Cm infection, but less IL-17 was secreted in TCRδ-/- mice than in WT mice on day 7. The intracellular cytokine staining analysis further indicated that the secretion of IL-17 by CD3+ CD4+ T cells in TCRδ-/- mice was significantly decreased as compared with that in WT mice on days 3 and 7 after Cm infection. Conclusion γδT cells protect mice from Chlamydia respiratory infection by promoting the Chlamydia-specific Th17 immune responses. Key words: Chlamydia muridarum; γδT cell; Th17 immune response