TY - JOUR
T1 - An in vitro comparison of commonly used topical glucocorticoid preparations
AU - Stellato, C.
AU - Atsuta, J.
AU - Bickel, C. A.
AU - Schleimer, R. R.
N1 - Funding Information:
Supported by grants from the National Institutes of Health and by gifts from Astra, Glaxo, and Schering-Plough.
PY - 1999
Y1 - 1999
N2 - Background: Glucocorticoids (GC) are potent inhibitors of peripheral blood eosinophil, basophil, and airway epithelial cell function. Objectives: We compared in vitro the inhibitory activity of synthetic GC used for topical treatment in asthma and rhinitis on basophil histamine release (HR), eosinophil viability, and klexpression of vascular cell adhesion molecule-1 (VCAM-1) in the human bronchial epithelial cell line BEAS-2B. Methods: Cells were treated for 24 hours with increasing concentrations (range 10-13 to 10-6 mol/L) of fluticasone propionate (FP), mometasone furoate (MF), budesonide (BUD), beclomethasone dipropionate (BDP), triamcinolone acetonide (TAA), hydrocortisone (HC), or dimethyl sulfoxide diluent before challenge. HR was measured by a fluorometric assay, viability of purified eosinophils was assessed by erythrosin B dye exclusion, and expression of VCAM-1 was measured by flow cytometry. Results: GC induced a concentration-dependent inhibition of anti-IgE-induced HR. Maximum inhibition ranged from 59.7% to 81 %, with a rank order of GC potency of FP > MF > BUD > BDP ≅ TAA ≫ HC. Three-day treatment of eosinophils with GC concentration-dependently inhibited IL-5-induced eosinophil viability, with a rank of potency almost identical to that observed with basophil HR. The rank order of potency of GC for inhibition of the expression of VCAM-1 in BEAS-2B cells was MF ≅ FP ≫ BUD > TAA > HC ≅ BDP. Inhibitory concentration of 50% values revealed that epithelial cells were the most sensitive and eosinophils were the least sensitive. Conclusions: These data, combined with information on pharmacodynamics of these drugs in vivo, may be useful in estimating GC local anti-inflammatory effects.
AB - Background: Glucocorticoids (GC) are potent inhibitors of peripheral blood eosinophil, basophil, and airway epithelial cell function. Objectives: We compared in vitro the inhibitory activity of synthetic GC used for topical treatment in asthma and rhinitis on basophil histamine release (HR), eosinophil viability, and klexpression of vascular cell adhesion molecule-1 (VCAM-1) in the human bronchial epithelial cell line BEAS-2B. Methods: Cells were treated for 24 hours with increasing concentrations (range 10-13 to 10-6 mol/L) of fluticasone propionate (FP), mometasone furoate (MF), budesonide (BUD), beclomethasone dipropionate (BDP), triamcinolone acetonide (TAA), hydrocortisone (HC), or dimethyl sulfoxide diluent before challenge. HR was measured by a fluorometric assay, viability of purified eosinophils was assessed by erythrosin B dye exclusion, and expression of VCAM-1 was measured by flow cytometry. Results: GC induced a concentration-dependent inhibition of anti-IgE-induced HR. Maximum inhibition ranged from 59.7% to 81 %, with a rank order of GC potency of FP > MF > BUD > BDP ≅ TAA ≫ HC. Three-day treatment of eosinophils with GC concentration-dependently inhibited IL-5-induced eosinophil viability, with a rank of potency almost identical to that observed with basophil HR. The rank order of potency of GC for inhibition of the expression of VCAM-1 in BEAS-2B cells was MF ≅ FP ≫ BUD > TAA > HC ≅ BDP. Inhibitory concentration of 50% values revealed that epithelial cells were the most sensitive and eosinophils were the least sensitive. Conclusions: These data, combined with information on pharmacodynamics of these drugs in vivo, may be useful in estimating GC local anti-inflammatory effects.
KW - Allergy
KW - Basophil
KW - Eosinophil
KW - Epithelial cells
KW - Glucocorticoids
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U2 - 10.1016/s0091-6749(99)70334-9
DO - 10.1016/s0091-6749(99)70334-9
M3 - Article
C2 - 10482838
AN - SCOPUS:0032825885
SN - 0091-6749
VL - 104
SP - 623
EP - 629
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 3 II
ER -