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目的通过测量支气管哮喘患者治疗前后支气管肺泡灌洗液(BALF)及血清 Clara 细胞分泌蛋白(CCSP)水平的变化,明确 Clara 细胞及其分泌蛋白在哮喘发病中的作用,探讨内源性抗炎机制,完善哮喘的气道炎症理论。方法选择健康对照组15人,哮喘急性发作期和缓解期病人各15例,留取静脉血和支气管肺泡灌洗液,用 ELISA 方法分别测定血清和 BALF 上清液中CCSP 的水平,同时测定患者肺功能用力肺活量(FVC)、一秒钟用力呼气容积的肺活量(FEVt)及呼气中段流量(MMEF),并对结果进行统计学分析。结果哮喘急性发作组和哮喘缓解组血清及 BALF 上清液 CCSP 水平显著低于健康对照组,P<0.05;哮喘急性发作组和哮喘缓解组血清及 BALF 上清液 CCSP 水平无统计学差异;哮喘急性发作组肺功能 FEV_1、FVC、MMEF 显于低于哮喘缓解组及健康对照组,P<0.01;哮喘缓解组及健康对照组肺功能 FEV_1、FVC、MMEF 值无统计学差异。直线相关分析表明,哮喘急性发作组血清和 BALF 上清液 CCSP 水平与 FEV_1呈高度正相关(相关系数分别为 r=0.798,P<0.01;r=0.762,P<0.01);哮喘缓解组患者血清和 BALF 上清液 CCSP 水平与 FEV_1呈正相关关系(r=0.645,P<0.01;r=0.716,P<0.01);健康对照组血清和 BALF 上清液 CCSP 水平与 FEV_1呈高度正相关(r=0.789,P<0.01;r=0.732,P<0.01)。哮喘急性发作组血清 CCSP 水平显著低于 BALF 上清液中 CCSP 水平,且两者呈高度正相关(r=0.875,P<0.01);哮喘缓解组血清 CCSP 水平显著低于 BALF上清液 CCSP 水平,两者呈高度正相关(r=0.936,P<0.01);健康对照组血清 CCSP 水平亦显著低于 BALF 上清液 CCSP 水平,两者亦呈高度正相关(r=0.825,P<0.01)。结论本研究结果提示 Clara 细胞分泌蛋白,参与了哮喘各期的发病机制,CCSP 变化可作为哮喘病情变化和治疗效果的指标之一。
Objective To investigate the role of Clara cells and secreted proteins in the pathogenesis of asthma by measuring the changes of secreted proteins (CCSP) in bronchoalveolar lavage fluid (BALF) and serum Clara cells before and after treatment in patients with bronchial asthma, and to explore the mechanism of endogenous anti-inflammatory , Improve asthma airway inflammation theory. Methods Fifteen healthy control subjects, 15 acute exacerbation and remission stage patients were enrolled in this study. Vein and bronchoalveolar lavage fluid were collected. The levels of CCSP in serum and BALF supernatant were determined by ELISA. FVC, FEVt and MMEF of the forced expiratory volume in one second, and the results were statistically analyzed. Results The levels of CCSP in serum and BALF supernatant of acute exacerbation group and asthma remission group were significantly lower than those in healthy control group (P <0.05). There was no significant difference in CCSP levels between acute asthma attack group and asthma remission group and BALF supernatant. Asthma The FEV 1, FVC and MMEF of lung function in acute attack group were lower than those in asthma remission group and healthy control group, P <0.01. There was no significant difference in FEV 1, FVC and MMEF between pulmonary remission group and healthy control group. Linear correlation analysis showed that CCSP level in serum and BALF supernatant of asthma exacerbation group was positively correlated with FEV_1 (r = 0.798, P <0.01, r = 0.762, P <0.01) (R = 0.645, P <0.01; r = 0.716, P <0.01). There was a positive correlation between the level of CCSP and the level of FEV_1 in serum and BALF supernatant of healthy controls (r = 0.789, P <0.01; r = 0.732, P <0.01). The levels of CCSP in asthma exacerbation group were significantly lower than that in BALF supernatant (r = 0.875, P <0.01). The serum CCSP level in asthma remission group was significantly lower than that in BALF supernatant (R = 0.936, P <0.01). The level of serum CCSP in healthy control group was also significantly lower than that in BALF supernatant (r = 0.825, P <0.01) . Conclusion The results of this study suggest that Clara cells secrete proteins involved in the pathogenesis of various stages of asthma. The change of CCSP may be used as one of the indicators of asthma changes and therapeutic effect.