细胞粘附分子在哮喘发病中作用的初步研究

PRIMARY STUDY ON THE EFFECT OF CELL ADHESION MOLECULE IN ASTHMA

目的：探讨β整合素家族及 Ｃ Ｄ４４粘附分子在哮喘发病中的作用。方法：用流式细胞仪检测哮喘豚鼠外周血单个核细胞（ Ｐ Ｂ Ｍ Ｃｓ）表面 Ｃ Ｄ１１ａ表达，分别用免疫酶标法（ Ａ Ｐ Ａ Ａ Ｐ）及流式细胞分析法检测哮喘患儿 Ｐ Ｂ Ｍ Ｃｓ表面 Ｃ Ｄ１１ａ、 Ｃ Ｄ１１ｂ 及 Ｃ Ｄ４４粘附分子表达。结果：①哮喘豚鼠 Ｐ Ｂ Ｍ Ｃｓ 表面 Ｃ Ｄ１１ａ表达明显高于对照组（ Ｐ＜ ００１），地塞米松可抑制 Ｃ Ｄ１１ａ表达；②哮喘急性发作期患儿 Ｐ Ｂ Ｍ Ｃｓ 表面 Ｃ Ｄ１１ａ、 Ｃ Ｄ１１ｂ及 Ｃ Ｄ４４粘附分子表达较正常人均明显增高（ Ｐ 均＜ ０００１），但与缓解期患儿相比无显著差异。结论： Ｃ Ｄ１１ａ、 Ｃ Ｄ１１ｂ 、 Ｃ Ｄ４４ 粘附分子参与了哮喘的病理生理过程，糖皮质激素可抑制粘附分子表达，发挥抗炎作用。

Objective:To investigate the role of β integin and CD 44 molecule in asthmatic airway inflammation.Methods:The expression of CD 11a molecule on peripheral blood mononuclear cell (PBMC) from guinea pig was detected by flow cytometry.The expression of CD 11a ,CD 11b and CD 44 on PBMC from the patients with asthma was detected by flow cytometry and APAAP assay,respectively.Results:①The expression of CD lla in the asthmatic guinea pigs was significantly higher than that in the controls ( P <0 01).Dexamethasone could inhibit the expression of CD 11a ;②The patients with acute exacerbation of asthma had higher percentages of CD 11a ,CD 11b and CD 44 compared with the controls ( P <0 01),but no difference from the relief asthmatic patients.Conclusion:Cell adhesion molecule play an important role in asthmatic airway inflammation.Glucocorticoid may inhibit airway inflammation via decreasing the expression of cell adhesion molecule.