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

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.