[Expression property of adhesive molecule ICAM-1 on vitro-cultured pulmonary microvascular endothelial cells under the stimuli of asthmatic serum].
It has been recognized only in the past 15 years that the major pathological mechanism of asthma is inflammation, which has a hallmark of focal leukocyte extravasation. The different recruitment behaviors of inflammatory cells depend on the expression of specific adhesive molecules on both leukocytes and endothelial cells (EC). Intercellular cellular adhesion molecule-1(ICAM-1) plays a major role. In the previous detailed in-vivo study of asthmatic models, we have proved the significant pathological increase of both the leukocyte-endothelium adhesion phenomenon and the ICAM-1 expression in the tissues of asthmatic lung. It may be due to an ICAM-1 accumulation on the microvascular endothelial cells and thus an enhancement of adhesion force during the course of disease. In this study, endothelial cells were obtained from rats by mechanical isolation of lung tissues and in vitro culture on glass. Confluent endothelial cells were incubated with serum collected from rat blood of normal and asthmatic models and were used for in vitro study of endothelial cell adhesion. The effect of pathological serum stimulation was examined on the expression of ICAM-1 of the pulmonary microvascular endothelial cells (PMEC). The expression of ICAM-1 on PMEC was measured by indirect immuno-fluorescence with flow cytometry. We found that the surface expression of ICAM-1 was obviously increased on serum-incubated EC as compared with that on the culture solution-incubated one, and that asthmatic serum increased the expression of ICAM-1 on EC to a peak in 4 hours and then decreased it rapidly, the expression level remained the same in the whole course when EC was treated with culture solution or normal serum.
Sheng
J
J
Beijing Polytechnic University, Beijing 100022.
Zeng
Y
Y
Zhuang
F
F
D000818:Animals; D001249:Asthma / Q000276:immunology*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D007106:Immune Sera / Q000494:pharmacology*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D008168:Lung / Q000166:cytology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D007106:Immune Sera; D018799:Intercellular Adhesion Molecule-1