短期慢性阻塞性肺疾病模型的免疫特点  

Immune characteristics of short-term chronic obstructive pulmonary disease model

作　　者：张寒晓 段荦 张牧之 张若旸 赵刘一诺 周若男 李运淇 吕喆[1] 王晶晶 袁慧慧[1] 崔烨 孙英[1] 王炜[1] Zhang Hanxiao;Duan Luo;Zhang Muzhi;Zhang Ruoyang;Zhao Liuyinuo;Zhou Ruonan;Li Yunqi;Lyu Zhe;Wang Jingjing;Yuan Huihui;Cui Ye;Sun Ying;Wang Wei(Department of Immunology,School of Basic Medical Science,Capital Medical University,Beijing 100069,China;Department of Laboratory Animal Sciences,Capital Medical University,Beijing 100069,China;Department of Pulmonary and Critical Care Medicine,Center of Respiratory Medicine,China-Japan Friendship Hospital,Beijing 100029,China,National Center for Respiratory Medicine,Beijing 100029,China)

机构地区：[1]首都医科大学基础医学院免疫学系,北京100069 [2]首都医科大学实验动物部,北京100069 [3]中日友好医院呼吸中心,呼吸与危重症医学科,国家呼吸医学中心,北京100029

出　　处：《首都医科大学学报》2023年第2期203-211,共9页Journal of Capital Medical University

基　　金：国家自然科学基金项目(82090013);北京市属高校高水平教师队伍建设支持计划高水平创新团队建设计划项目(IDHT20190510)。

摘　　要：目的 分析短期烟草烟雾暴露后肽段激发的慢性阻塞性肺疾病模型小鼠的免疫特点。方法 建立上述短期慢性阻塞性肺疾病模型,行肺组织石蜡切片和支气管肺泡灌洗液分类计数观察气道炎症;有创肺功能检测肺呼吸力学参数;借助Luminex技术分析细胞因子表达情况;流式细胞术检测小鼠肺组织中辅助T(T helper,Th)细胞和固有淋巴样细胞(innate lymphoid cells,ILCs)亚群的数量及比例变化。结果 短期烟草烟雾暴露后肽段激发可损伤小鼠肺泡;诱导以中性粒细胞浸润为主的气道炎症;3型细胞因子表达增高;Th17、ILC3细胞增多,ILC1、ILC2细胞减少。结论 烟草烟雾暴露后肽段激发诱导的短期慢性阻塞性肺疾病模型以3型免疫为主,且ILC3可能比Th17的作用更为重要。Objective To analyze the immune characteristics of short-term chronic obstructive pulmonary disease(COPD)model induced by peptide challenge after smoking exposure.Methods A short-term murine model of COPD was established by smoking sensitization and peptide infusion challenge.Airway inflammation was analyzed by histological staining sections of lung tissues and cells of bronchoalveolar lavage fluid.An invasive lung function test was used to measure changes of lung respiratory mechanical parameters in experimental mice.The Luminex instrument platform was employed to quantify concentrations of cytokines in lung homogenates.Flow cytometry was used to measure changes in the numbers and proportions of subsets of T helper(Th)cells and innate lymphoid cells(ILCs)in mouse lung tissues.Results The data showed that short-term tobacco smoke exposure and peptide challenge caused damage of the alveoli,induced airways inflammation with neutrophil infiltration,increased the expression of type 3 cytokines and the numbers of Th17 and ILC3,while decreased proportion of ILC1 and ILC2.Conclusion The short-term COPD models of smoke sensitization and peptide challenge are dominated by type 3 immunity,in which ILC3 may play a more important role than Th17.

关 键 词：慢性阻塞性肺疾病 烟草烟雾 固有淋巴样细胞 

分 类 号：R392[医药卫生—免疫学]