EXPRESSION AND MODULATION OF ADHESION MOLECULES ON HUMAN BRONCHIAL EPITHELIAL-CELLS

Epithelial damage in the airways is a feature often observed in patien ts with asthma and is probably caused by the interaction of epithelial cells with leukocytes. As adhesion molecules are thought to be import ant in this interaction, we analyzed the expression and modulation of adhesion molecules on primary cultured human bronchial epithelial cell s and the bronchial epithelial cell lines BEAS-2B and NCI-H-292. E-sel ectin, P-selectin, and VCAM-1 were absent under basal and stimulated c onditions. The adhesion molecules ICAM-1 (CD54), LFA-3 (CD58), and CD4 4 (H-CAM) were expressed basally on primary cultured human bronchial e pithelial cells and the BEAS-2B and NCI-H-292 cell lines. CD44 and LFA -3 expression did not change after stimulation with IFN-gamma or TNf-a lpha. In contrast, ICAM-1 expression on human bronchial epithelial cel ls and BEAS-2B cells could be increased by incubation with PMA, IFN-ga mma, TNF-alpha, and especially with the combination of IFN-gamma and T NF-alpha. The maximal ICAM-1 expression on both epithelial cell types was obtained with the combination of TNF-alpha and IFN-gamma after 48 h of incubation. The NCI-H-292, cell line was different in that it onl y showed increased ICAM-1 expression after stimulation with PMA and IF N-gamma and not by the combination of IFN-gamma and TNF-alpha or with TNF-alpha alone. In conclusion, the bronchial epithelial cells tested express several adhesion molecules, but only ICAM-1 expression was inf luenced by inflammatory cytokines.