Biochemical analysis of glucocorticoid-induced inhibition of IgE-mediated histamine release from mouse mast cells

M. Daeron, A. R. Sterk, F. Hirata, T. Ishizaka

Research output: Contribution to journalArticlepeer-review

Abstract

Pretreatment of mouse mast cells with 10-7 to 10-6 M dexamethasone (DM) during overnight sensitization with mouse IgE antibody resulted in inhibition of antigen-induced histamine release and degranulation. The inhibition of both degranulation and histamine release increased linearly with the duration of the treatment; maximal inhibition was obtained after approximately 16 hr with DM. The addition of DM to sensitized mast cells immediately before antigen challenge did not affect the antigen-induced histamine release. DM interacted directly with mast cells by binding to DM-specific cytoplasmic receptors. The treatment of mast cells with DM did not affect the binding of IgE to mast cells or intracellular cAMP levels. Bridging of cell-bound IgE anti-DNP antibody on mouse mast cells eithers by multivalent DNP-HSA or by anti-IgE induced phospholipid methylation at the plasma membrane and Ca++ influx into the cells. Pretreatment of mast cells with DM inhibited the antigen-induced phospholipid methylation and Ca++ uptake but failed to affect histamine release by Ca++ ionophore A23187. The results suggest that DM treatment inhibits histamine release by the inhibition of the early stage of biochemical processes leading to opening Ca++ channels but does not affect the process distal to Ca++ influx or the binding of IgE molecules to IgE receptors.

Original languageEnglish (US)
Pages (from-to)1212-1218
Number of pages7
JournalJournal of Immunology
Volume129
Issue number3
StatePublished - Jan 1 1982

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Biochemical analysis of glucocorticoid-induced inhibition of IgE-mediated histamine release from mouse mast cells'. Together they form a unique fingerprint.

Cite this