Dexamethasone Does Not Modulate Eosinophil Adhesion to Endothelial Cells

Abstract

Background: Glucocorticoids are representative agents in the anti-inflammatory treatment of allergic airway diseases. Although they reduce the number of tissue eosinophils, its exact mechanism has not been completely established. Objective: The present study was undertaken to evaluate whether dexamethasone modulates the adhesive property of eosinophils. The effect on the expression of endothelial adhesion molecules was also evaluated. Methods: Blood eosinophils from healthy subjects were incubated in the presence or absence of 0.1–1 µM of dexamethasone for 6 h at 37°C. Eosinophil chemotaxis and adhesion to paraformaldehyde-fixed human pulmonary vascular endothelial cells (HPMEC) were then examined. The effects of dexamethasone on the expression of VCAM-1 and ICAM-1 on HPMEC were examined by cell ELISA. Results: 1 µM dexamethasone significantly inhibited the chemotactic response of eosinophils to 1 µM formyl-methionyl-leucyl-phenylalanine (FMLP). On the other hand, dexamethasone did not modify either the spontaneous or FMLP-stimulated adhesion of eosinophils to resting HPMEC. Similarly, dexamethasone did not alter either the spontaneous adhesion of eosinophils to or the expression of VCAM-1 or ICAM-1 on HPMEC stimulated with IL-4 + TNF-α. Conclusion: Dexamethasone does not modify the adhesive property of eosinophils or the expression of adhesion molecules on endothelial cells. Thus, it is unlikely that glucocorticoids directly modulate the adhesive interaction between eosinophils and endothelial cells.