IL-10通过上调socs3抑制衣原体感染细胞炎症因子表达
IL-10 inhibits expression of inflammatory factors in Chlamydia-infected cells by up-regulating socs3
罗玲艳 1杜昆1
作者信息
- 1. 长江大学附属第一医院输血科,荆州 434000
- 折叠
摘要
目的:研究SOCS3蛋白在IL-10抑制衣原体感染细胞炎症因子表达中的作用及其机制.方法:采用Western blot技术检测IL-10对衣原体感染细胞STAT3蛋白活化的影响,以及在socs3 siRNA作用下p38及ERK1/2活化情况;RT-PCR技术检测衣原体感染细胞在IL-10或Stattic作用下socs3基因表达情况;ELISA检测衣原体感染细胞在socs3 siRNA作用下,炎症因子IL-6和IL-12产生情况.结果:IL-10可以通过激活STAT3蛋白上调socs3基因表达;衣原体能诱导IL-6及IL-12产生,但IL-10可以通过上调socs3基因表达抑制IL-6及IL-12产生;SOCS3蛋白能抑制p38和ERK1/2通路活化.结论:IL-10通过诱导SOCS3蛋白抑制p38和ERK1/2通路活化,从而抑制炎症因子的产生.
Abstract
Objective:To investigate the role and mechanisms of SOCS3 protein in IL-10 inhibiting the expression of inflam-matory factors in Chlamydia-infected cells.Methods:The activation of STAT3 protein were examined in Chlamydia-infected cells by Western blot,and the activation of p38 and ERK1/2 were also examined in infected cells treated with socs3 siRNA.The expression of socs3 gene was examined in Chlamydia-infected cells treated with IL-10 or Stattic by RT-PCR.IL-6 and IL-12 were measured in infect-ed cells treated with socs3 siRNA using ELISA kits.Results:Socs3 expression was up-regulated by IL-10 through activation of STAT3 protein.IL-6 and IL-12 induced by Chlamydia were down-regulated by IL-10 through induction of socs3.The activation of p38 and ERK1/2 signalling pathways were inhibited by SOCS3.Conclusion:IL-10 inhibits the production of pro-inflammatory cytokines through induction of SOCS3 and inhibition p38 and ERK1/2 signalling pathways.
关键词
沙眼衣原体/炎症因子/白细胞介素10/细胞因子信号转导抑制因子Key words
Chlamydia trachomatis/Inflammatory factors/IL-10/SOCS引用本文复制引用
出版年
2024
国家科技期刊平台
NSTL
万方数据