中文摘要：

目的建立沙眼衣原体（Chlamydiatrachomatis，Ct）D型感染小鼠生殖道动物模型，为研究人类生殖道ct感染的病理变化和致病机制提供实验基础。方法分离20个临床株，经阴道接种C3H／HeJ小鼠，得到清除时间明显延长的临床株（UT0603）。应用该临床株建立ctD型感染模型，免疫荧光检测阴道脱落上皮细胞中衣原体的含量；原位组织免疫荧光检测上生殖道的衣原体感染定植情况；分离生殖道组织，肉眼观察并进行病理学评分。结果ct临床株感染小鼠下生殖道其排菌量及排菌周期明显延长，可见衣原体有上行感染和定植，并能引发类似人类生殖道感染的病理变化。结论成功建立了CtD型生殖道感染动物模型。

英文摘要：

Objective To construct a mouse model for studying pathophysiology and mechanism of human Chlamydia trachomatis genital infection. Methods Innate immunity-deficient C3H/HeJ female mice were infected intravaginally with human C. trachomatis serovar D urogenital isolates for screening the highest violent clinical strain. The clinical strain UT0603 as well as standard strain D/UW-3/CX were then used to reinfect naive mice, the lower genital tract shedding were monitored by swabbing every 3-7 day over the entire infection period by culture. Some mice were sacrificed at early infection stage to detection of in site Chlamydia growth by immunofiuoreseence assay, then all the mice were sacrificed at later infection stage to evaluate upper genital tract gross pathology and histopathological characterization. Results In the lower genital tract, Chlamydia shedding time course were significantly prolonged in clinical strain infected mice. Chlamydia not only growth in the lower genital tract, the live organism also ascending and growth in the upper genital tissue. The gross appearance under naked eyes and dilation and inflammation scores under microscope all showed that the genital tract pathology from the clinical strain infected mice were much more severe than standard strain infected control mice. Conclusion Together, all these results demonstrated that a mouse model for Chlamydia genital infection was constructed.