The Study On Th17 And Treg Responses And The Cross Regulation Between Th17 And Treg Responses During Cm Lung Infection

Objective:To investigate the level of Th17 and Treg responses and the cross regulation between Th17 and Treg responses during Cm lung infection.Methods:C57BL/6 mice, female, aged 6-8 weeks were inoculated intranasally with 1×103 IFUs of Cm to build the murine model of pneumonia. The body weight changes, mortality, pathogenesis and the growth of Cm in the lung were monitored to determine the severity of the disease. Mice were sacrificed at the different days following infection. To determine the Th17 and Treg responses in mice, intracellular cytokine staining was used to assay the proliferation of Th17 cells and Treg cells in the spleen; RT-PCR was used to assay the mRNA expression of IL-17, TGF-βand their transcription factors ROR-γt and FOXp3 in the lung. Anti-mouse IL-17 and CD25 mAbs were used to neutralize the function of Th17 cells and Treg cells following Cm lung infection. Mice were sacrificed at day 7 post-infection.The severity of the disease was monitored to determine the role of Th17 and Treg in Cm lung infection.The proliferation of Treg cells and Th17 cells in the spleen was assayed by intracellular cytokine staining;the mRNA expression of IL-17, TGF-βand their transcription factors ROR-γt and FoxP3 in the lung was assayed by RT-PCR, The results were analysised to investigate the role of Th17 and Treg and the cross regulation between them during Cm lung infection.Results:Intranasally infected with 1×103 IFUs of Cm in mice resulted in chlamydial mouse pneumonitis featured by body weight lost, chlamydia growth and severe pathological damage in the lung. High levels of Th17 and Treg responses were induced by Cm lung infection. Include:the proliferation of Th17 cells and Treg cells upregulation in the spleen; high levels of the IL-17 and TGF-βmRNA expression and their transcription factors ROR-γt and FoxP3 expression in the lung. What is important:the IL-17 and CD25 neutralized mice exhibited greater body weight lost, more organism growth and much more serious pathological damage. But, compared with PBS control mice, the proliferation of Treg cells and Th17 cells in the spleen and the expression of TGF-β,IL-17 and their transcription factors FoxP3, ROR-γt in the lung were not changed in the IL-17and CD25 neutralized mice.Conclusion: Intranasally infected of Cm resulted in typical chlamydial mouse pneumonitis.Cm lung infection induced high levels of Th17 and Treg responses. Th17 and Treg enduced protective function in Cm lung infection. But the cross regulation between Th17 and Treg were not manifest.