肠道衣原体诱导CD8+T细胞协同生殖道衣原体致病的机制研究

衣原体是常见的性传播病原体，能够导致输卵管性不孕，严重危害生殖健康。近期发现衣原体也可在肠道检出并引起不孕不育，但其致病机制不明。我们前期研究表明，肠道衣原体能通过CD8+T细胞促进小鼠输卵管积水的发生，同时肠道衣原体感染小鼠的生殖道组织内可检出更多分泌促纤维化因子的细胞，推测肠道衣原体通过诱导致病性CD8+T细胞促进输卵管的损伤和纤维化。基于上述基础，本课题拟利用小鼠肠道衣原体感染模型，应用感染示踪及免疫细胞过继转移等微生物与免疫学技术，探索肠道衣原体诱导的CD8+T细胞协同生殖道衣原体致病的具体机制，明确CD8+T细胞在肠道衣原体促进生殖道病变中的作用。该课题的开展将进一步阐明肠道衣原体的致病机制并为其导致的不孕不育的临床诊疗提供重要的科学依据。

Chlamydia is a common sexually transmitted pathogen, which causes tubal infertility and exerts serious threats to reproductive health. Recent studies have found that chlamydia can colonize gastrointestinal (GI) tract and induce infertility through unknown mechanisms. Our previous studies have shown that chlamydia in GI tract promoted hydrosalpinx by CD8+T cells. And more cells secreting fibrogenic factor were detected in the genital tract tissues of mice with chlamydial GI infection. We proposed that GI tract colonized chlamydia promoted tubal damage and fibrosis by inducing pathogenic CD8+T cells. Based on these previously results, mice with chlamydial GI infection and microbial and immunological techniques such as pathogen tracing and immune cells adoptive transfer were used to explore the specific mechanism of GI tract chlamydia induced CD8+T cells promoting chlamydial genital pathogenesis. We aimed to clarify the role of GI colonized chlamydia induced CD8+T cells in promoting genital chlamydia induced hydrosalpinx. This study will help to understand the pathogenic mechanism of chlamydia and provide important scientific evidence for clinical diagnosis and treatment of infertility induced by GI tract chlamydia infection.