Effect of steroids on immunoglobulin-induced eosinophil degranulation

Hirohito Kita, Randa Abu-Ghazaleh, Colin J. Sanderson, Gerald J. Gleich

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)70-77
Number of pages8
JournalThe Journal of allergy and clinical immunology
Volume87
Issue number1 PART 1
DOIs
StatePublished - 1991
Externally publishedYes

Fingerprint

Eosinophils
Immunoglobulins
Steroids
Interleukin-5
Glucocorticoids
Secretory Immunoglobulin A
Dihydrotestosterone
Methylprednisolone
Dexamethasone
Hydrocortisone
Estradiol
Eosinophil-Derived Neurotoxin
Immunoglobulin G
Ovalbumin
Sepharose
Radioimmunoassay
Asthma
Cell Culture Techniques
Hormones
Inflammation

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Effect of steroids on immunoglobulin-induced eosinophil degranulation. / Kita, Hirohito; Abu-Ghazaleh, Randa; Sanderson, Colin J.; Gleich, Gerald J.

In: The Journal of allergy and clinical immunology, Vol. 87, No. 1 PART 1, 1991, p. 70-77.

Research output: Contribution to journalArticle

Kita, Hirohito ; Abu-Ghazaleh, Randa ; Sanderson, Colin J. ; Gleich, Gerald J. / Effect of steroids on immunoglobulin-induced eosinophil degranulation. In: The Journal of allergy and clinical immunology. 1991 ; Vol. 87, No. 1 PART 1. pp. 70-77.
@article{bab67387e8df4f7f94d990df5d18e9fc,
title = "Effect of steroids on immunoglobulin-induced eosinophil degranulation",
abstract = "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.",
author = "Hirohito Kita and Randa Abu-Ghazaleh and Sanderson, {Colin J.} and Gleich, {Gerald J.}",
year = "1991",
doi = "10.1016/0091-6749(91)90214-9",
language = "English (US)",
volume = "87",
pages = "70--77",
journal = "Journal of Allergy and Clinical Immunology",
issn = "0091-6749",
publisher = "Mosby Inc.",
number = "1 PART 1",

}

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.

PY - 1991

Y1 - 1991

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.

UR - http://www.scopus.com/inward/record.url?scp=0025877188&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025877188&partnerID=8YFLogxK

U2 - 10.1016/0091-6749(91)90214-9

DO - 10.1016/0091-6749(91)90214-9

M3 - Article

VL - 87

SP - 70

EP - 77

JO - Journal of Allergy and Clinical Immunology

JF - Journal of Allergy and Clinical Immunology

SN - 0091-6749

IS - 1 PART 1

ER -