沙眼衣原体泌尿生殖道感染是近年来国内外最常见、并发症众多、迁延难治、疫苗乏效的性传播疾病，是国际疾病控制的热点难点。我们前期发现噬菌体衣壳蛋白Vp1对衣原体特异抑制率达65%-92%，并在小鼠生殖道衣原体感染模型中验证。单一蛋白对衣原体抑制如此明显，说明其抑制机制并非以往噬菌体机械性裂解而是通过未知信号通路诱发产生类似凋亡的现象。我们进一步发现衣原体表面的PmpI是该通路触发点，Vp1结合后导致衣原体TCS和T3SS水平升高。进而推测Vp1作用于PmpI的信号通过TCS或T3SS传达，最终激活衣原体死亡相关蛋白(CADD)和蛋白水解酶反向破坏自身。本课题旨在前期基础上运用穿梭质粒和Group II Intron技术，结合抑制后不同时相免疫电镜、蛋白质谱和生物信息学分析等，研究衣原体及其蛋白变化与PmpI、TCS、T3SS的关系，阐明抑制性信号通路、发现抑制效应标志、探索衣原体“凋亡”机制。

Chlamydia trachomatis urogenital infection is the most common sexually transmitted disease in the world. Protracted Chlamydia trachomatis urogenital infection, which is international hotspots and difficulties, has many complications and lack of effective vaccines. We previously found that the suppression / destruction rate of Phage capsid protein Vp1 against chlamydia reached 65%-92%. Vp1 can promote the genital tract Chlamydia clearance in mouse model. The inhibition of Chlamydia by single Vp1 protein is so obvious that the mechanism is not the mechanical lysis of bacteriophage, but a special pathway induce the similar "apoptosis" phenomenon. So far there is no report on the related signaling pathways. Furthermore we found that the PmpI protein of the outer membrane of Chlamydia trachomatis is the trigger point of the inhibitory signal pathway resulting in elevated levels of TCS and T3SS after Vp1 binding. Therefore, we hypothesize that this pathway led to reverse self destruction of Chlamydia trachomatis by CADD and proteolytic enzyme. The purpose of this study is to disclose the relationship between PmpI, TCS and T3SS and the changes of the protein level after Chlamydia repressed, elucidate the inhibitory signal pathway, search for the inhibitory effect of marker proteins and explore the ‘apoptosis’ mechanism in chlamydia by using the shuttle plasmid and Group II Intron technology, combined with protein mass spectra ,immunoelectron microscopy analysis of different time point and bioinformatics method.