沙眼衣原体热休克蛋白60致小鼠宫颈炎的研究

中华皮肤科杂志 ›› 2011, Vol. 44 ›› Issue (8): 596-598.

沙眼衣原体热休克蛋白60致小鼠宫颈炎的研究

蔡微¹,刘隽华²,陈木开³,李海翩⁴,韩建德⁵

1. 福州市皮肤病防治院
2. 中山大学附属第一医院黄埔院区皮肤科
3. 中山大学附属第一医院
4. 广州中山大学附属第一医院
5. 广州市中山大学第一医院皮肤科

收稿日期:2010-09-06 修回日期:2011-04-15 出版日期:2011-08-15 发布日期:2011-07-26
通讯作者: 韩建德 E-mail:hanjd_gzb@21cn.net
基金资助:
沙眼衣原体热休克蛋白60与上生殖道感染的相关性研究

Chlamydia trachomatis heat shock protein 60 （cHSP60） induces murine cervicitis

Received:2010-09-06 Revised:2011-04-15 Online:2011-08-15 Published:2011-07-26
Contact: HAN JIANDE E-mail:hanjd_gzb@21cn.net

摘要/Abstract

摘要：

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cHSP60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 cHSP60、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 cHSP60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。cHSP60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cHSP60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。

关键词: 疾病模型, 动物

Abstract:

Objective To investigate the role of cHSP60 in the pathogenesis of murine cervicitis. Methods Fifty female C3H/HeN mice were randomly and equally classified into 5 groups, including the control group receiving no treatment and 4 groups receiving intravaginal inoculation of cHSP60 （cHSP60 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 cHSP60 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 cHSP60 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 cHSP60 and MoPn groups （all 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 cHSP60 may be a primary pathogenic factor in chlamydial genital tract infection.

Key words: Disease models, animal

蔡微刘隽华陈木开李海翩韩建德. 沙眼衣原体热休克蛋白60致小鼠宫颈炎的研究[J]. 中华皮肤科杂志, 2011, 44(8): 596-598.

参考文献

References: [1] Gerbase A C, Rowley J T, Heymann D H, et al. Global prevalence and incidence estimates of selected curable STDs.[J]. Sex Transm Infect,1998,74 Suppl 1:S12-S16. [2] Nelson H D, Helfand M. Screening for chlamydial infection.[J]. Am J Prev Med,2001,20(3 Suppl):95-107. [3] 不孕妇女宫颈沙眼衣原体感染的临床观察[J]. 实用妇产科杂志,2002(03). [4] Peeling R W, Patton D L, Cosgrove S Y, et al. Antibody response to the chlamydial heat-shock protein 60 in an experimental model of chronic pelvic inflammatory disease in monkeys (Macaca nemestrina).[J]. J Infect Dis,1999,180(3):774-779. [5] den Hartog J E, Land J A, Stassen F R, et al. Serological markers of persistent C. trachomatis infections in women with tubal factor subfertility.[J]. Hum Reprod,2005,20(4):986-990. [6] Domeika M, Domeika K, Paavonen J, et al. Humoral immune response to conserved epitopes of Chlamydia trachomatis and human 60-kDa heat-shock protein in women with pelvic inflammatory disease.[J]. J Infect Dis,1998,177(3):714-719. [7] Shemer Y, Sarov I. Inhibition of growth of Chlamydia trachomatis by human gamma interferon.[J]. Infect Immun,1985,48(2):592-596. [8] Rodriguez N, Fend F, Jennen L, et al. Polymorphonuclear neutrophils improve replication of Chlamydia pneumoniae in vivo upon MyD88-dependent attraction.[J]. J Immunol,2005,174(8):4836-4844. [9] van Zandbergen G, Gieffers J, Kothe H, et al. Chlamydia pneumoniae multiply in neutrophil granulocytes and delay their spontaneous apoptosis.[J]. J Immunol,2004,172(3):1768-1776. [10] Bartels C, Maass M, Bein G, et al. Detection of Chlamydia pneumoniae but not cytomegalovirus in occluded saphenous vein coronary artery bypass grafts.[J]. Circulation,1999,99(7):879-882. [11] Quinn T C, Gaydos C A. In vitro infection and pathogenesis of Chlamydia pneumoniae in endovascular cells.[J]. Am Heart J,1999,138(5 Pt 2):S507-S511. [12] Rupp J, Kothe H, Mueller A, et al. Imbalanced secretion of IL-1beta and IL-1RA in Chlamydia pneumoniae-infected mononuclear cells from COPD patients.[J]. Eur Respir J,2003,22(2):274-279. [13] Register K B, Davis C H, Wyrick P B, et al. Nonoxidative antimicrobial effects of human polymorphonuclear leukocyte granule proteins on Chlamydia spp. in vitro.[J]. Infect Immun,1987,55(10):2420-2427. [14] Gueinzius K, Magenau A, Erath S, et al. Endothelial cells are protected against phagocyte-transmitted Chlamydophila pneumoniae infections by laminar shear stress Gueinzius: Shear stress protects from C. pneumoniae infection.[J]. Atherosclerosis,2008,198(2):256-263. [15] Equils O, Lu D, Gatter M, et al. Chlamydia heat shock protein 60 induces trophoblast apoptosis through TLR4.[J]. J Immunol,2006,177(2):1257-1263. [16] Smith S C, Baker P N, Symonds E M. Increased placental apoptosis in intrauterine growth restriction.[J]. Am J Obstet Gynecol,1997,177(6):1395-1401. [17] Allaire A D, Ballenger K A, Wells S R, et al. Placental apoptosis in preeclampsia.[J]. Obstet Gynecol,2000,96(2):271-276.