嗜酸粒细胞性支气管炎与支气管哮喘患者诱导痰黏蛋白水平的差异机制研究

Difference in sputum concentrations of mucin in eosinophilic bronchitis and asthma

目的:分析嗜酸粒细胞性支气管炎(EB)与哮喘患者的诱导痰黏蛋白水平的差异并探讨其差异机制。方法:通过ELISA法检测20例EB、哮喘患者及正常对照的痰上清液黏蛋白MUC5AC、MUC5B及LTC4和PGE2水平,分析上述炎症介质在EB与哮喘患者的黏蛋白差异机制中所起的作用。结果:哮喘组的MUC5AC[(26.8±8.5)μg/m L]显著高于EB组[(17.6±7.0)μg/m L]和对照组[(12.5±4.3)μg/m L](P<0.01),MUC5B[(1.1±0.5)μg/m L]与EB组[(2.6±0.5)μg/m L]和对照组[(2.6±0.4)μg/m L]相比,显著降低(P<0.01),EB组的MUC5AC和MUC5B水平与对照组比较差异无显著性(P>0.05)。与其他组相比,哮喘组的LTC4[(700.8±172.3)pg/m L]和EB组的PGE2[(433.8±118.1)pg/m L]均显著升高(P<0.01)。受试者的痰上清LTC4与MUC5AC呈正相关(r=0.785,P<0.01),与MUC5B呈负相关(r=-0.703,P<0.01)。结论:哮喘与EB患者的大气道黏蛋白MUC5AC与MUC5B的比例存在显著差异,而LTC4和PGE2之间的失衡可能是引起该差异的机制。

Objective To investigated the difference in induced sputum concentrations of mncin between the patients with eosinophilic bronchitis （EB） and classic asthma, and found out the difference in mechanism. Methods 20 patients with eosinophilic bronchitis （EB）, 20 patients with classic asthma and 10 healthy controls were enrolled. Induced sputum levels of MUC5AC, MUC5B, LTC4 and PGE2 were measured by enzyme immunoassay in patients and healthy control. Results In patients with asthma, sputum MUC5A （26.8±8.5）μg/mL and LTC4 （700.8±172.3）pg/mL were significantly elevated whereas MUC5B levels （1.1 ± 0.5）μg/mL were reduced compared with patients with EB MUC5AC： （17.6± 7.0）μg/mL, LTC4：（320.9 ± 89.4）pg/mL, MUC5B： （2.6 ± 0.5）μg/mL and healthy controls MUC5AC： （12.5±4.3）μg/mL, LTC4：（91.2±16.1）pg/mL, MUC5B： （2.6 ± 0.4）μg/mL （P 〈 0.01）. PGE2 levels were higher in patients with EB （433.8 ± 118.1）pg/mL than in asthma（172.7± 74.5）pg/mL and controls（113.3 ± 18.3）pg/mL（P 〈 0.01）, but results did not differ between asthma and controls. The LTC4 showed a significant positive correlation with MUC5AC （r = 0.785 ,P 〈 0.01 ）, and a significant negative correlation with MUC5B （r = -0.703 ,P 〈 0.01 ）. Conclusion A significant difference in MUC5AC/MUC5B ratio was founded in proximal airway between EB and asthma. The unbalance level between LTC4 and PGE2 would be involved in the pathogenesis of airway mucus hypersecretion.