Chlam ydia mu ridra um respiratory tract infection induces the proliferation ofγδT cells and the secre-t ion of IFN-γand IL-17 / 中华微生物学和免疫学杂志

ABSTRACT

Objective To investigate the proliferation, activation and cytokine production of γδT cells during different periods of Chlamydia muridarum ( Cm) respiratory tract infection. Methods C57BL/6 mice were inoculated intranasally with 3×103 inclusion-forming units(IFU)of Cm strains to induce the murine model of chlamydial pneumonitis.Mononuclear cells were isolated from lung tissue samples col-lected from mice at different time points after infection.Flow cytometry analysis was used to detect the per-centages of CD3+TCRγδ+T cells in lung tissues and the expression of CD69 molecule.Intracellular cytokine staining was performed to analyze the secretion of IL-17 and IFN-γbyγδT cells.Results The mouse model of chlamydial pneumonitis was successfully established by intranasal inoculation of C57BL/6 mice with 3×103 IFU of Cm strains.Compared with the mice without Cm infection, the percentage and the absolute number of CD3+TCRγδ+T cells in mice lung tissues were significantly increased after Cm infection, the peak of which was reached on the 7th day, followed by a decline.The expression of CD69 molecule onγδT cells isolated from mice lung tissues reached to the highest level on the third day after Cm infection and declined slightly afterwards.Moreover, enhanced secretion of IL-17 and IFN-γby γδT cells were observed in mice with Cm infection and the highest levels of the two cytokines were detected on the third day after infection. Most of the cytokines ( IL-17 and IFN-γ) were secreted by γδT cells rather than by αβT cells in the early stage of Cm infection.However, the CD3+CD4+T cells were more capable of producing IFN-γand IL-17 thanγδT cells after three days of Cm infection.Conclusion Cm respiratory tract infection could induce the aggregation and activation ofγδT cells at the infection site.TheγδT cells were the predominant cells produ-cing IL-17 and IFN-γin the early stage of host anti-chlamydia response.