IL-17在沙眼衣原体呼吸道感染早期表达及与衣原体复制的关系

Early IL-17 production in airway upon Chlamydia trachomatis infection and its relationship with chlamydial organism replication

目的探讨炎症性细胞因子IL-17在沙眼衣原体呼吸道感染中的早期表达及与衣原体复制的关系。方法128只小鼠按随机数字表法分为实验组和对照组,实验组用4000包涵体形成单位(IFU)沙眼衣原体小鼠肺炎株(MoPn)通过鼻腔感染小鼠,对照组则给予等量蔗糖磷酸盐缓冲液(SPG),分别在感染后0、1、1.5、2、3、4、8、12d处死小鼠,用免疫荧光检测(IFA)衣原体在肺组织中的生长情况,通过ELISA检测小鼠肺组织IL-17表达。24只小鼠分为3组,分别用160、800、4000IFUMoPn通过鼻腔感染小鼠,于感染后第2天测定肺组织中衣原体生长及IL-17表达。16只小鼠随机分为2组,用4000IFUMoPn通过鼻腔感染小鼠,实验组肌肉注射利福平和氯霉素,对照组则给予等量PBS,于感染后第2天测定肺组织中衣原体生长及IL-17表达。结果MoPn感染后第1天,肺组织有衣原体生长,于感染后第8天达高峰。感染后第2天,IL-17在小鼠肺组织中的表达达峰值,并很快下降。仅剂量为4000IFUMoPn感染小鼠2d后,肺组织中同时有衣原体生长和IL-17的表达。经抗生素处理后衣原体生长被抑制,同时也检测不到IL-17的表达。结论IL-17在衣原体呼吸道感染早期出现,其表达情况与衣原体感染剂量和早期复制有关。

Objective To evaluate the early IL-17 production in airway upon Chlamydia trachomatis infection and its relationship with chlamydial organism replication. Methods A total of 128 mice were randomly divided into experimental groups and control ones. The mice in experimental groups were induced by intranasal inoculation with Chlamydia trachomatis mouse pneumonitis （MoPn, now classified as a new species C. muridarurm biovar with 4000 IFU of MoPn. The same volume of SPG was given to the control ones. Chlamydial growth in the lung was assessed by inoculating HeLa cell monolayer with lung homogenates followed by IFA at 0, 1 , 1.5, 2, 3, 4, 8 and 12 d after infection. Meanwhile, IL-17 was measured by ELISA. Another 24 mice were divided randomly into 3 groups and infected with 160, 800, and 4 000 IFU of MoPn by intranasal inoculation, respectively. Chlamydial growth and IL-17 production in the lung were assessed at 2 d after infection. Another 16 mice were divided into experimental and control groups and were administrated with 4 000 IFU of MoPn by intranasal injection with or without rifampicin and ehloromycepin treatment. Chlamydial growth and IL-17 production in the lung were also assessed at 2 d after infection. Results Chlamydial growth in the lung was found at 1 d after infection, and reached its peak at 8 d with subsequent decline in quantity. IL-17 peaked at 48 h transiently, and then decreased subsequently. Both Chlamydial growth and IL-17 production in the lung were detectable at 2 d after infection only with, 4 000 IFU of MoPn by intranasal administration. Chlamydial growth in the lung was blocked by treatment with antibiotics. Meanwhile, no IL-17 was detectable by ELISA. Conclusion IL-17 can be produced early in airway upon Chlamydia trachomatis. IL-17 production may be associated with the dose of Chlamydia trachomatis infection and early chlamydial organism replication.