沙眼衣原体热休克蛋白60致小鼠宫颈炎的研究

Chlamydia trachomatis heat shock protein 60 （criSP60） induces murine cervicitis

目的研究沙眼衣原体热休克蛋白60（cHsP60）在小鼠宫颈炎发病中的作用。方法50只雌性C3H／HeN小鼠随机分成5组（每组10只），其中一组为空白对照组，其余4组分别设为criSP60组、活体鼠肺炎衣原体（MoPn）组、灭活MoPn组及生长培养基组，该4组通过自制接种器通过阴道内分别接种criSP60、MoPn、灭活MoPn及生长培养基，第5天时，取小鼠宫颈组织行病理检查，观察宫颈局部的组织学变化并评分。结果criSP60组10只小鼠中9只宫颈黏膜可见不同程度的以中性粒细胞为主的炎症细胞聚集及黏膜细胞坏死、脱落等炎症反应，与活体MoPn组病理特征相同。criSP60组小鼠宫颈炎症发生率为90％，中性粒细胞计数为76．00（25．0—80．0），炎症评分为12．5（11．5—14．25），MoPn组分别为80％、25．00（8．75～32．5）和9．00（8．00～11．5），两组比较，差异均无统计学意义（P〉0．05）；灭活MoPn组分别为40％、0．00（0．00—15．50）和0．00（0．00—12．50），宫颈黏膜炎症反应较弱，炎症评分及炎症发生率均低于criSP60组及MoPn组，差异均有统计学意义（P〈0．05）。生长培养基组仅2只小鼠出现黏膜浅层少量中性粒细胞游入。结论cHSP60是沙眼衣原体宫颈炎发病的重要致病物质。

Objective To investigate the role of criSP60 in the pathogenesis of marine cervicitis. Methods Fifty female C3H/HeN mice were randomly and equally classified into 5 groups, including the con- trol group receiving no treatment and 4 groups receiving intravaginal inoculation of criSP60 （criSP60 group）, live elementary bodies of Chlamydia trachomatis mouse pneumonitis （MoPn group）, inactive elementary bodies of MoPn （inactive MoPn group） and growth medium （medium group）, respectively. Five days after the inoculation, cervical tissue was resected from these mice and subjected to pathological examination. Results There were varying degrees of inflammatory reaction characterized by neutrophil infiltration, necrosis and shedding of mucosal cells in the cervices of mice in criSP60 and MoPn groups. No statistical difference was observed in the incidence of cervicitis （90% vs. 80%, P 〉 0.05）, neutrophile count [76.00 （25.0 - 80.0） vs. 25.00 （8.75 - 32.5）, P〉 0.05] or inflammation score [12.5 （11.5 - 14.25） vs. 9.00 （8.00- 11.5）, P〉 0.05] between the cHSPdO and MoPn group. The inflammatory reaction was weak with decreased incidence of cervicitis （40%）, inflammation score [0.00 （0.00 - 12.50）] and neutrophile count [0.00 （0.00 - 15.50）] in inactive MoPn group compared with the criSP60 and MoPn groups Call P 〈 0.05）. A small number of neutrophils migrated into the superficial layer of cervical mucosa in only 2 mice in the medium group. Conclusion criSP60 may be a primary pathogenic factor in chlamydial genital tract infection.