中文摘要：

目的探讨肺炎嗜衣原体(Chlamydophila pneumoniae,Cpn)热休克蛋白(heat shock protein,HSP)10(CHSP10)诱导人单核细胞分泌炎症因子的作用及Toll样受体(Toll-like receptor,TLR)2、TLR4与此作用的相关性。方法以去内毒素活性的不同质量浓度CHSP10(0.5、1、5、10、20、30μg/ml)刺激THP-1细胞0、6、12、24、36、48、60 h,检测蛋白未处理组、加热处理组、去蛋白处理组中IL-1β及IL-6水平;用CHSP10刺激C3H系野生型(C3H/HeN)和TLR4缺陷型(C3H/HeJ)小鼠腹腔巨噬细胞,分别检测IL-1β及IL-6水平;用CHSP10刺激被抗TLR2/TLR4抗体处理的THP-1细胞,检测IL-1β、IL-6的变化。结果 CHSP10可诱导THP-1细胞产生炎症因子IL-1β、IL-6;CHSP10诱生C3H系野生型小鼠细胞分泌的炎症因子明显高于TLR4缺陷型小鼠细胞;用TLR2和/或TLR4抗体封闭后,CHSP10诱生的IL-1β、IL-6不同程度减少。结论 CHSP10可能作为炎症相关蛋白参与了Cpn对宿主细胞的致炎作用;并且TLR2及TLR4在该炎症刺激信号的传递过程中发挥一定的作用。

英文摘要：

To investigate the role and mechanism of heat shock protein 10(HSP10) of Chlamydophila pneumoniae in inducing inflammatory reaction.Purified native recombinant HSP10 from C.pneumoniae(CHSP10) were inactivated for cleaning contaminated endotoxin and were used to stimulate THP-1 with different concentrations for different time,then the cytokines levels were measured by using human enzyme-linked immunosorbent assay kit.Peritoneal macrophages from TLR4-deficient mice and wide-type mice were stimulated with endotoxin-free proteins respectively,and the cytokines levels were measured.Furthermore,blocking experiments with neutralizing anti-human TLR2 or/and TLR4 MAb were carried out and ELISA was used to detect the concentration of cytokines.Result showed that HSP10 was able to induce IL-1β and IL-6 secretion in THP-1.Wild-type macrophages from C3H/HeN secreted higher IL-1β and IL-6 level compared with macrophages from TLR4-deficient mice after stimulation with HSP10,and the level of HSP10-induced proinflammatory cytokines decreased in blocking experiments compared with untreated control.In conclusion,HSP10 may be involved in the pathogenesis of C.pneumoniae-induced inflammation,while TLR2 and TLR4 appear to be involved in CHSP10-mediated expression of IL-1β and IL-6.