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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。
Objective To investigate the effect of heat shock protein 10 (CHSP10) induced by Chlamydophila pneumoniae (Cpn) on the secretion of inflammatory cytokines by human monocytes and the effects of Toll-like receptor (TLR) 2, Correlation of TLR4 with this effect. Methods THP-1 cells were stimulated with CHSP10 (0.5, 1, 5, 10, 20, 30μg / ml) with different concentrations of endotoxin for 0,6,12,24,36,48 and 60 h, The levels of IL-1β and IL-6 in the group of heat-treated and the deproteinised groups were measured. The peritoneal macrophages of C3H / HeN and C3H / HeJ mice were stimulated by CHSP10, IL-1|Â and IL-6 were measured. The THP-1 cells treated with anti-TLR2 / TLR4 antibody were stimulated with CHSP10 to detect the changes of IL-1|Â and IL-6. Results CHSP10 induced THP-1 cells to produce inflammatory cytokines IL-1β and IL-6. The inflammatory cytokines secreted by CHSP10-induced wild-type C3H mice were significantly higher than that of TLR4-deficient mice. TLR2 and / After blocking, CHSP10-induced IL-1β, IL-6 decreased to varying degrees. Conclusion CHSP10 may be involved in the inflammatory cytokines as a proinflammatory cytokine induced by Cpn. TLR2 and TLR4 play a role in the signal transduction of inflammatory stimuli.