Non-genomic effect of glucocorticoids on inhibition of expression of CD63 on peripheral blood basophils

Background: Glucocorticoids (GC) could inhibit histamine release from rat peritoneal mast cells within 10 minutes, which classical genomic mechanism could not explain. The clinical efficacy of inhaled corticosteroids combined with long-acting beta 2-agonists has been widely demonstrated in asthma. Objective: In order to validate the benefit of the combined these agents in vitro, we studied a rapid effect of fluticasone propionate (FP) and formoterol (FORM) alone and in-combination on inhibition of expression of CD63, which is a maker of degranulation of basophils, in house dust mite (HDM)-sensitive patients with asthma. Methods: Whole peripheral bloods from asthmatic patients were incubated with HDM for 20 min in the pretreatment of FP and/or FORM for 1 hour. We assessed the expression of CD63 on basophils by quantifying the mean fluorescence of CD63 in IgE-positive cells by FACS analysis. Results: A high concentration of FP (10 -8 M) alone, but not a low concentration of FP (10 -12 M) alone, inhibits CD63 expression-induced with HDM. The combination of FP (10 -8 M) and FORM (10 -7 M) more inhibits CD 63 expression on basophils. Conclusion: The study provided evidence that non-genomic mechanism might be involved in rapid effect of glucocorticoids on basophils in asthma.