首都医科大学学报 ›› 2023, Vol. 44 ›› Issue (2): 203-211.doi: 10.3969/j.issn.1006-7795.2023.02.004

• 呼吸系统疾病免疫学研究进展 • 上一篇    下一篇

短期慢性阻塞性肺疾病模型的免疫特点

张寒晓1#, 段荦1#, 张牧之1, 张若旸1,3, 赵刘一诺1, 周若男1, 李运淇1,  吕喆1, 王晶晶2, 袁慧慧1, 崔烨1, 孙英1, 王炜1*
  

  1. 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
  • 收稿日期:2023-01-24 出版日期:2023-04-21 发布日期:2023-04-17
  • 通讯作者: 王炜 E-mail:wy_robin@ccmu.edu.cn
  • 基金资助:
    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)

Immune characteristics of short-term chronic obstructive pulmonary disease model

Zhang Hanxiao1#, Duan Luo1#, Zhang Muzhi1, Zhang Ruoyang1,3, Zhao Liuyinuo1, Zhou Ruonan1, Li Yunqi1, Lyu Zhe1, Wang Jingjing2,  Yuan Huihui1, Cui Ye1,Sun Ying1,Wang Wei1*   

  1. 1.Department of Immunology, School of Basic Medical Science, Capital Medical University, Beijing 100069, China; 2. Department of Laboratory Animal Sciences, Capital Medical University,Beijing 100069, China; 3. 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
  • Received:2023-01-24 Online:2023-04-21 Published:2023-04-17
  • Supported by:
    This study was supported by National Natural Science Foundation of China(82090013),High-level Teacher Team Building Support Plan for High-level Innovation Team Building Plan in Beijing Municipal Universities(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。

关键词: 慢性阻塞性肺疾病, 烟草烟雾, 固有淋巴样细胞

Abstract:

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.

Key words: chronic obstructive pulmonary disease, cigarette smoke, innate lymphoid cells

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