TY - JOUR
T1 - Effect of steroids on immunoglobulin-induced eosinophil degranulation
AU - Kita, Hirohito
AU - Abu-Ghazaleh, Randa
AU - Sanderson, Colin J.
AU - Gleich, Gerald J.
N1 - Funding Information:
From the *Department of Immunology, the **Allergic Diseases Research Laboratory, Mayo Clinic and Mayo Foundation, Roch-ester, Minn., and ***National Institute for Medical Research, Mill Hill, London, England. Supported by National Institutes of Health Grants AI 15231 and AI 09728, and from the Mayo Foundation. Received for publication Feb. 20, 1990. Revised Sept. 11, 1990. Accepted for publication Sept. 11, 1990. Reprint requests: Gerald J. Gleich, MD, Department of Immunol-ogy, Mayo Clinic, Rochester, MN 55905.
PY - 1991/1
Y1 - 1991/1
N2 - Because glucocorticoids are a mainstay in the treatment of asthma and other allergic diseases, we tested the effect of various steroid hormones on secretory IgA- and IgG-induced eosinophil degranulation in vitro. Human normodense eosinophils were purified by discontinuous Percoll density gradient, and hypodense eosinophils were obtained by culture of normodense cells with recombinant human interleukin (rIL)-5. Eosinophils were incubated with various steroids, including dexamethasone, hydrocortisone, methylprednisolone, estradiol, or dihydrotestosterone at concentrations from 10-9 to 10-4 mol/L. Sepharose 4B beads coupled to ovalbumin, secretory IgA, or IgG were added as targets of degranulation and incubated at 37 ° C for 4 hours. In some experiments, rIL-5 was added to eosinophils before addition of beads to activate the cells. The release of eosinophil-derived neurotoxin was measured by radioimmunoassay as an index of degranulation. Dexamethasone (10-9 to 10-4 mol/L), hydrocortisone (10-9 to 10-4 mol/L), estradiol (10-9 to 10-7 mol/L), and dihydrotestosterone (10-9 to 10-4 mol/L) had no effect on normodense eosinophil degranulation. Methylprednisolone, 10-5 mol/L, inhibited degranulation of normodense eosinophils up to 20%, whereas 10-4 mol/L inhibited degranulation of hypodense eosinophils, up to 30%, Overall, no difference in inhibition by steroids was observed between normodense and hypodense eosinophils. rIL-5 enhanced immunoglobulin-induced eosinophil degranulation, but this effect of rIL-5 was not blocked by any of the steroids tested. These results suggest that eosinophil degranulation and rIL-5-mediated eosinophil activation are not direct targets of glucocorticoids and that the beneficial effects of glucocorticoids on allergic inflammation in vivo are not likely due to direct effects on eosinophil degranulation.
AB - Because glucocorticoids are a mainstay in the treatment of asthma and other allergic diseases, we tested the effect of various steroid hormones on secretory IgA- and IgG-induced eosinophil degranulation in vitro. Human normodense eosinophils were purified by discontinuous Percoll density gradient, and hypodense eosinophils were obtained by culture of normodense cells with recombinant human interleukin (rIL)-5. Eosinophils were incubated with various steroids, including dexamethasone, hydrocortisone, methylprednisolone, estradiol, or dihydrotestosterone at concentrations from 10-9 to 10-4 mol/L. Sepharose 4B beads coupled to ovalbumin, secretory IgA, or IgG were added as targets of degranulation and incubated at 37 ° C for 4 hours. In some experiments, rIL-5 was added to eosinophils before addition of beads to activate the cells. The release of eosinophil-derived neurotoxin was measured by radioimmunoassay as an index of degranulation. Dexamethasone (10-9 to 10-4 mol/L), hydrocortisone (10-9 to 10-4 mol/L), estradiol (10-9 to 10-7 mol/L), and dihydrotestosterone (10-9 to 10-4 mol/L) had no effect on normodense eosinophil degranulation. Methylprednisolone, 10-5 mol/L, inhibited degranulation of normodense eosinophils up to 20%, whereas 10-4 mol/L inhibited degranulation of hypodense eosinophils, up to 30%, Overall, no difference in inhibition by steroids was observed between normodense and hypodense eosinophils. rIL-5 enhanced immunoglobulin-induced eosinophil degranulation, but this effect of rIL-5 was not blocked by any of the steroids tested. These results suggest that eosinophil degranulation and rIL-5-mediated eosinophil activation are not direct targets of glucocorticoids and that the beneficial effects of glucocorticoids on allergic inflammation in vivo are not likely due to direct effects on eosinophil degranulation.
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U2 - 10.1016/0091-6749(91)90214-9
DO - 10.1016/0091-6749(91)90214-9
M3 - Article
C2 - 1991924
AN - SCOPUS:0025877188
SN - 0091-6749
VL - 87
SP - 70
EP - 77
JO - The Journal of Allergy and Clinical Immunology
JF - The Journal of Allergy and Clinical Immunology
IS - 1 PART 1
ER -