摘要
目的 :为了探讨支气管上皮细胞 (brochialepithlialcells,BECs)炎症过程中一些具有保护作用的调节因子的调节效应 ,建立有效的细胞研究模型。方法 :用臭氧 (O3)应激建立细胞损伤模型 ,观察O3应激引起的BECs与中性粒细胞 (polymorphonuclearleukocyte ,PMNs)、嗜酸性粒细胞 (eosinophil,EOS)黏附的影响 ,及在炎症损伤中的作用 ;同时观察ICAM 1抗体对黏附的阻断及ICAM 1蛋白的表达。结果 :O3应激可增加BECs与PMNs、EOS的黏附率 ,产生应激反应 ;抗细胞间黏附分子 1(intercellularadhesionmolecule ,ICAM 1)抗体能阻断BECs与PMNs ,EOS的黏附 ;O3应激使ICAM 1蛋白表达增加。结论 :O3应激引起气道炎症 ,且介导BECs与PMNs,EOS黏附的黏附分子是ICAM 1。
Objective To determine into the inflammation process of bronchial epithelial cells (BECs) and observe the modulatory effect of some protective factors on BECs. Methods We built the cell injury model with ozone and observed the effect of ozone stress on polymorphonuclear loeukocyte (PMNs) and eosinophil (EOS) adhesion to BECs. The effect of intercellular adhesion molecule(ICAM 1) antibody on the adhesion and ICAM 1 protein expression of BECs was observed at the same time. Results O 3 increased the adhesion of BECs to PMNs and EOS. Adhesion could be blocked by ICAM 1 antibody, suggesting ICAM 1 was the principal molecule leading PMNs and EOS adhesion to BECs. The immunocytochemistry assay indicated that O 3 incresed the expression of ICAM 1 protein of BECs. Conclusion Ozone stress leads to inflammation, and the principal adhesion molecule is ICAM 1 resulting in adhesion between BECs and PMNs, and between BECs and EOS.
出处
《湖南医科大学学报》
CSCD
北大核心
2002年第3期192-194,共3页
Bulletin of Hunan Medical University
基金
国家自然科学基金资助课题 (3 9770 63 5 )
