支气管哮喘与PBMC上CD11a、CD18、CD44分子表达的关系  

Relationship of Expression of β-Integrin and CD44 Molecules with the Pathophysiology of Brochial Asthma

作　　者：张劭夫[1] 张波[1] 徐德斌[1] 

机构地区：[1]济南军区总医院呼吸科,济南250031

出　　处：《上海免疫学杂志》2002年第1期54-55,共2页Shanghai Journal of Immunology

摘　　要：本文探讨 β整合素家族及CD44粘附分子在哮喘发病中的作用。采用流式细胞仪分别检测哮喘豚鼠外周血单个核细胞(PBMC )表面CD11a分子及哮喘患者PBMC表面CD18和CD44等分子的表达情况。结果 :(1)哮喘豚鼠PBMC表面CD11a分子表达明显高于对照组 (P <0 0 1) ,地塞米松可抑制CD11a表达 ;(2 )哮喘患者PBMC表面CD18、CD44表达较正常人明显增高 (P <0 0 1)。使细胞粘附分子参与了哮喘的病理生理过程 ,糖皮质激素可抑制细胞粘附分子表达 ,发挥抗炎作用。In order to investigate the role of β integrin and CD44 in the pathophysiology of bronchial asthma,the expression of CD11a on PBMC of guinea pigs and those of CD18 and CD44 on PBMC of asthmatics were detected by using flow cytometry. The results showed that expression of CD11a was significantly higher than that in the control,and dexamethasome could inhibit this expression. On the other hand,asthmatics showed higher percentages of CD18 and CD44 than those of the controls. These results suggest that cell adhesion molecules may play an important role on asthmatic airway inflammation,and glucocorticoid inhibit airway inflammations by decreasing the expression of these molecules.

关 键 词：细胞粘附分子 支气管哮喘 外周血单核细胞 CD11A CD18 CD44 

分 类 号：R562.25[医药卫生—呼吸系统]