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Abstract
Beclomethasone, budesonide, dexamethasone, and fluticasone propionate enhanced human eosinophil apoptosis in a concentration-dependent manner in vitro as assessed by flow cytometric analysis and morphological analysis. The order of potency was fluticasone propionate (EC 50 3.7±1.8 nM)≈budesonide (EC 50 5.0±1.7 nM)>beclomethasone (EC 50 51±19 nM)>dexamethasone (EC 50 303±40 nM). Hydrocortisone, prednisolone, and prednisone (up to 1 μM) did not induce any significant increase in eosinophil apoptosis. The apoptosis promoting effects of glucocorticoids on eosinophils were reversed by an antagonist of glucocorticoid receptor mifepristone. The survival-prolonging effect of tumor necrosis factor (TNF)-α was reversed by dexamethasone and fluticasone (1 μM). In contrast, fluticasone, and dexamethasone (1 μM) did not reverse the survival-prolonging effects of interleukins-3 and -5 or granulocyte-macrophage colony-stimulating factor (GM-CSF). The results suggest that fluticasone and budesonide induce eosinophil apoptosis at clinically achievable drug concentrations via an effect on glucocorticoid receptor.
Published Version
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