细颗粒物通过诱导小鼠γδT/Th17细胞分泌白细胞介素-17A加剧肺部炎症  

Interleukin-17A-producingγδT/Th17 cells exacerbate fine particulate matter-induced lung inflammation

作　　者：侯文肖 吴依娜[1] 丛鲁红[3] 李涛[1] 张洪春[4] 段军[1] HOU Wen-xiao;JIANG Meng;CONG Lu-hong(Surgical Intensive Care Unit,China-Japan Friendship Hospital,Beijing 100029,China)

机构地区：[1]中日友好医院外科重症医学科,北京100029 [2]北京中医药大学研究生院,北京100029 [3]中日友好医院教育处,北京100029 [4]中日友好医院保健医疗部,北京100029

出　　处：《中日友好医院学报》2021年第4期220-222,234,F0003,共5页Journal of China-Japan Friendship Hospital

基　　金：国家自然科学基金面上项目(81774265);北京协和医学院“中央高校基本科研”项目(3332019115)。

摘　　要：目的:明确白细胞介素17A(IL-17A)是细颗粒物(PM2.5)导致的肺损伤过程中的重要炎症因子,并探究此过程中产生IL-17A的关键细胞类型。方法:准备30只C57BL/6J小鼠和15只IL-17A基因敲除(IL-17A^(-/-))C57BL/6J小鼠,将15只野生型小鼠作为对照组,另外15只野生型小鼠和15只IL-17A^(-/-)小鼠作为实验组,用2mg/ml浓度的PM2.5气管内滴注造模,持续9d。对照组和实验组中各5只小鼠分别在模型构建的第3d、6d、9d处死,将其肺组织和肺泡灌洗液进行形态学、流式、PCR和ELISA检测。结果:实验组野生型小鼠和对照组在第3d、6d、9d时γδT和Th17细胞的增加有显著差异(P<0.05)。ELISA检测,与实验组IL-17A^(-/-)小鼠相比,实验组野生型小鼠第9d IL-1β、TNF-α水平有显著差异(均P<0.05),且第9d的HE染色提示实验组IL-17A^(-/-)小鼠比实验组野生型小鼠肺组织中的炎性细胞浸润明显减少。结论:PM2.5可通过诱导小鼠γδT和Th17细胞分泌IL-17A,从而加剧肺部炎症反应。Objective:To probe into the possible role of interleukin-17 A(IL-17 A)and explore the key cell types that secrete IL-17 A in mouse models of PM2.5-induced lung injury.Methods:We purchased 30 Male C57 BL/6 J mice and 15 IL-17 A knockout(IL-17 A^(-/-))C57 BL/6 J mice.The mice in the experimental group(15 wild type[WT]mice and 15 IL-17 A^(-/-)mice)were subjected to intratracheal instillation of 2 mg/ml PM2.5 using normal saline.The model construction lasted for 9 days.Five mice in the control,WT and IL-17 A^(-/-)groups were,respectively,euthanized on the 3 rd,6 th and 9 th day of model construction.Then,lung tissue and alveolar lavage fluid were extracted for subsequent experiments.Results:At the 3 rd,6 th and 9 th day post-model establishment,the number ofγδT and Th17 cells showed a gradual increase in the lung tissues of PM2.5-treated mice(P<0.05).The expression of inflammatory factors IL-1βand TNF-αin the supernatant of alveolar lavage fluid were detected by ELISA,which suggested that the levels of IL-17 A,IL-1βand TNF-αwere significantly increased after 9 days of PM2.5-induced model establishment(P<0.05).Further study in IL-17 A^(-/-)mice revealed that knockout of IL-17 A could reduce inflammatory cell infiltration in lung tissues at the 9 th day of PM2.5-induced model establishment.Conclusion:IL-17 A-producingγδT and Th17 cells exacerbate PM2.5-induced lung inflammation.

关 键 词：细颗粒物 白细胞介素17A γδT/Th17细胞 肺部炎症反应 

分 类 号：R332[医药卫生—人体生理学]