Cristiana Stellato, MD, PhDa, Jun Atsuta, MD, PhDb, Carol A

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Presentation transcript:

An in vitro comparison of commonly used topical glucocorticoid preparations Cristiana Stellato, MD, PhDa, Jun Atsuta, MD, PhDb, Carol A. Bickel, MSa, Robert P. Schleimer, PhDa Journal of Allergy and Clinical Immunology Volume 104, Issue 3, Pages 623-629 (September 1999) DOI: 10.1016/S0091-6749(99)70334-9 Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 1 Inhibition of basophil histamine release with GC. Basophils were cultured for 24 hours in presence of indicated GC or DMSO diluent and subsequently challenged with 0.1 μg/mL anti-IgE. Data shown are mean ± SEM inhibition of histamine release (HR) from 2 to 6 experiments; percent HR induced by anti-IgE in DMSO-treated cells was 36.1% ± 12.2%. Journal of Allergy and Clinical Immunology 1999 104, 623-629DOI: (10.1016/S0091-6749(99)70334-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 2 Titration of IL-5 concentration used to prolong eosinophil survival (representative of n = 7 for IL-5 titration). Eosinophils were incubated with the indicated concentrations of IL-5 for 3 days in the presence of medium alone, DMSO diluent, or BUD (10–7 mol/L). Eosinophil viability was assessed by erythrosin B dye exclusion. Viability of cells is expressed as percent of total cells counted. Journal of Allergy and Clinical Immunology 1999 104, 623-629DOI: (10.1016/S0091-6749(99)70334-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 3 Inhibition of eosinophil survival by GC. Eosinophils were cultured for 3 days in medium containing 0.01 ng/mL rhu-IL-5 in presence of indicated concentrations of GC, DMSO diluent, or medium alone. Viability in DMSO-treated cells was 62% ± 10%. Results shown are mean ± SEM of n = 6. Journal of Allergy and Clinical Immunology 1999 104, 623-629DOI: (10.1016/S0091-6749(99)70334-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 4 Correlation among potencies of GCs in inhibiting basophil HR and eosinophil viability. Journal of Allergy and Clinical Immunology 1999 104, 623-629DOI: (10.1016/S0091-6749(99)70334-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 5 Inhibition of VCAM-1 expression on BEAS-2B epithelial cells. BEAS-2B cells were preincubated with various concentrations of GC for 24 hours before stimulation with 10 ng/mL of TNF-α for another 24 hours. Expression of VCAM-1 was measured by flow cytometry. Results shown are means ± SEM of n = 3. (Reprinted from Atsuta J, Plitt J, Bochner BS, Schleimer RP. Inhibition of VCAM-1 expression in human bronchial epithelial cells by glucocorticoids. Am J Respir Cell Mol Biol 1999;20:643-50. Used with permission.) Journal of Allergy and Clinical Immunology 1999 104, 623-629DOI: (10.1016/S0091-6749(99)70334-9) Copyright © 1999 Mosby, Inc. Terms and Conditions

Fig. 6 Comparison of IC50 values obtained for various GCs for inhibition of basophil histamine release, eosinophil survival, and expression of VCAM-1 on bronchial epithelial cell line BEAS-2B. Asterisk, P < .05 compared with HC; pound sign, P < .05 compared with BDP; two asterisks, P < .05 compared with TAA. Journal of Allergy and Clinical Immunology 1999 104, 623-629DOI: (10.1016/S0091-6749(99)70334-9) Copyright © 1999 Mosby, Inc. Terms and Conditions