目的观察慢性阻塞性肺疾病( COPD )模型大鼠调节性T细胞( Treg)、Th17细胞的变化。方法将30只大鼠随机均分为正常组、模型组。模型组采用烟熏加脂多糖( LPS)气管滴入方法建立COPD肺气虚证大鼠模型,模型复制成功第28天,采用动物肺功能仪检测大鼠肺功能,酶联免疫吸附法检测大鼠血清白细胞介素( IL)-1β、IL-10、IL-17、IL-35水平,免疫组化法检测肺组织FoxP3、IL-17表达,流式细胞术检测外周血Treg表达。结果模型组大鼠肺泡腔及肺间质内大量炎性细胞浸润,肺组织结构破坏。与正常组比较,模型组大鼠肺功能参数0.3 s用力呼气容积( FEV0.3)、用力肺活量(FVC)、FEV0.3/FVC值降低(P<0.01,P<0.05)；模型组大鼠血清IL-1β、IL-17、肺组织IL-17表达升高,血清IL-10、IL-35、肺组织FoxP3、外周血CD4+CD25+ Treg表达降低(P <0.01,P <0.05)；相关性分析显示,肺功能参数FEV0.3、FEV0.3/FVC、最大呼气流量( PEF)分别与IL-1β、IL-17呈负相关,与IL-35、FoxP3及CD4+CD25+Treg呈正相关( P <0.05)。结论 COPD 存在高炎症反应, CD4+CD25+Treg、Th17表达失衡,调节功能降低,导致炎症反应升高。%Objective To observe the change of regulatory T cells ( Treg) and Th17 cells in rat model of chronic obstructive pulmonary disease ( COPD) . Methods 30 rats were randomly divided into normal group, and model group. In addition to the normal group, the remaining rats were smoked plus lipopolysaccharide ( LPS) tracheal in-stillation method to establish COPD lung deficiency rat model. 28 days after the model copied, pulmonary function was tested using animals seized spirometer, interleukin (IL)-1β, IL-10, IL-17, IL-35 in serum were detected by enzyme-linked immunosorbent assay, FoxP3, IL-17 was detected in lung tissue by immunohistochemistry staining. Treg of peripheral was detected by flow cytometry. Results A large number of inflammatory cell infiltration and pulmonary alveolar interstitial intrinsic in rat model group. Compared with normal group, lung function parameters such as FEV0.3, FVC, FEV0.3/FVC were decreased in model group (P<0.01,P<0.05);IL-1β, IL-17 were in-creased, expression of IL-17 in serum, IL-10, IL-35, FoxP3, CD4+ CD25+ Treg were reduced (P<0.01,P<0.05). Correlation analysis showed that lung function parameters FEV0.3, FEV0.3/FVC, PEF, and IL-1β, IL-17 were negative correlattion respectively, IL-35, FoxP3 and CD4 +CD25 +Treg were positive correlation (P<0.05). Conclusion There is high inflammatory response in COPD. The high inflammatory response is caused by the im-balanced expression of CD4 +CD25 +Treg and Th17, which leads to increase in inflammatory response.
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