内源性IL-17诱导MIP-2与IL-6表达在衣原体肺炎中促进中性粒细胞循环

目的 探讨衣原体肺炎中白细胞介素-17（interleukin -17,IL-17）对中性粒细胞（polymorphonuclear leucocyte,PMN）循环的调节作用及机制.方法 用40 μl含1×10^3包涵体形成单位（inclusion-forming units,IFU）的衣原体鼠肺炎株（Chlamydia muridarum,Cm）呼吸道感染BALB/c小鼠,诱导鼠衣原体肺炎.用抗鼠IL-17单克隆抗体吸入中和内源性IL-17,以相应独特型抗体（IgG2α）作为对照.用RT-PCR检测小鼠肺组织及肺上皮细胞系巨噬细胞炎性蛋白-2 （macrophage inflammatory protein-2,MIP-2）和IL-6 mRNA的表达.取小鼠支气管肺泡灌洗液细胞染色计数PMN,感染肺组织进行病理染色.结果 衣原体肺炎中,内源性IL-17中和小鼠肺组织PMN浸润显著降低,支气管肺泡灌洗液PMN数量显著低于对照组.IL-17与TNF-α协同可上调肺上皮细胞MIP-2和IL-6 mRNA表达,且内源性IL-17中和小鼠肺组织MIP-2和IL-6表达显著降低.结论 衣原体肺炎中IL-17通过促进肺组织细胞分泌趋化性细胞因子MIP-2和前症性细胞因子IL-6,诱导PMN循环,参与宿主抗衣原体炎性应答.

Endogenous IL-17 Prompts Neutrophils Circulation through Inducing the Expression of MIP-2 and IL-6

Objective To investigate the regulation and mechanism of IL-17 to the neutrophil circulalion in mice chlamydia pneumonitis. Method BALB/c mice were inoculated intranasally with 1 × 10^3 inclusion-forming units （IFUs） of Chlamydia muridarum （Cm） . For endogenous IL-17 neutralization, some mice were intranasally administered with 10 μg of anti-mouse IL-17 mAb or isotype antibody （IgG2a） . The mRNA expression of ehemokine MIP-2 and cytokine IL-6 in the lung and pulmonary epithelial cells were detected by RT-PCR. Neutrophils numbers were determined by counting BAL cells. The lung tissue was stained for immunopathology. Results Compared to isotype control mice following Cm infection, there was less neutrophils infiltration in the lung of endogenous IL-17 neutralized mice. MIP-2 and IL-6 mRNA expression were up-regulated in pulmonary epithelial cells cuhured with the stimulation of mouse recombinant IL-17 and TNF-α. MIP-2 and IL-6 expression in lung tissue were significantly decreased. Conclusion IL-17 prompts the neutrophils circulation by inducing the expression of chemokine MIP-2 and cytokine IL-6 in the lung in chlamydial pneumonitis.