白细胞介素17C通过IKK/NF-κB通路调控慢性鼻窦炎的作用机制

Preliminary study on the mechanism of interleukin-17C regulating chronic sinusitis through IKK/NF-kB pathway

[目的]探讨白细胞介素17C(IL-17C)通过IKK/NF-κB通路调控慢性鼻窦炎(CRS)的作用机制,旨在为临床治疗CRS提供参考.[方法]选择IL-17C刺激人鼻黏膜原代上皮细胞(HNEPCs),采用CCK-8法检测不同质量浓度的IL-17C对HNEPCs活力的影响;利用ELISA法检测IL-17C诱导的HNEPCs中相关因子的表达水平;采用Western blot法检测IL-17C诱导的HNEPCs中IKK/NF-κB信号通路中相关蛋白的表达情况.[结果]与对照组比较,不同质量浓度的IL-17C对HNEPCs活力无显著影响(P>0.05);IL-17C干预组HNEPCs中IL-4、IL-5、IL-13、IL-17及p-IKK表达水平均明显升高,差异均具有统计学意义(P<0.05);IL-17C干预组HNEPCs中p-IKK、p-IκBα及p-NF-κB表达均明显升高(P<0.05),IKK、IκBα及NF-κB蛋白表达无明显改变(P>0.05).与IL-17C干预组比较,IL-17C+地塞米松组p-IKK、p-IκBα及p-NF-κB蛋白表达均明显降低(P<0.05).[结论]IL-17C可诱导HNEPCs中Th2及Th17相关炎症因子的产生,机制认为可能是调控IKK/NF-κB信号通路.

OBJECTIVE To investigate the mechanism of interleukin-17C(IL-17C)in regulating chronic rhinosinusitis(CRS)through IKK/NF-kB pathway,aiming to provide reference for clinical treatment of CRS.METHODS IL-17C was selected to stimulate primary cultured human nasal mucosal epithelial cells(HNEPCs).The effect of different mass concentrations of IL-17C on HNEPCs viability was detected by CCK-8.ELISA was used to detect the expression levels of related factors,and Western blot was used to detect the expressions of IKK/NF-kB signaling pathway-related proteins in HNEPCs induced by IL-17C.RESULTS Compared with the control group,IL-17C had no significant effect on the cell viability of HNEPC(P>0.05).The expression levels of IL-4,IL-5,IL-13,IL-17 and P-IKK in HNEPCs of the IL-17C intervention group were significantly increased,and the differences were statistically significant(P<0.05).The expressions of p-IKK,p-IkBαand p-NF-kB in HNEPCs of the IL-17C intervention group were significantly increased(P<0.05),while the expressions of IKK,IkBa and NF-kB were not significantly changed(P>0.05).Compared with the IL-17C intervention group,the protein expressions of p-IKK,p-IkBa and p-NF-kB proteins in the IL-17C+dexamethasone group were significantly decreased(P<0.05).CONCLUSION IL-17C can induce the production of Th2 and Th17 related infammatory factors in HNEPCs,the mechanism might be through the regulation of IKK/NF-kB signaling pathway.