INHIBITION OF IMMUNOGLOBULIN, BUT NOT POLYPEPTIDE BASE-STIMULATED RELEASE OF HISTAMINE AND ARACHIDONIC-ACID BY ANTI-INFLAMMATORY STEROIDS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 230  (1) , 175-182
Abstract
Incubation overnight of purified rat mast cells with glucocorticoids inhibited the release of histamine and [1-14C]arachidonic acid (and its metabolites) stimulated by 3 IgE-like secretagogs, anti-IgE, the antigen ovalbumin and concanavalin A. Pretreatment with glucocorticoids did not affect either histamine or [1-14C]arachidonic acid release stimulated by somatostatin, compound 48/80 [4-methoxy-N-methylbenzeneethanamine formaldehyde condensation product] or the Ca ionophore A23187 [calcimycin]. Glucocorticoids inhibited IgE-like arachidonic acid and histamine release with an order of potency similar to their in vivo anti-inflammatory potencies (i.e., fluocinolone > dexamethasone > hydrocortisone > cortisone). This inhibition required several hours and was temperature-dependent, suggesting a specific glucocorticoid receptor mechanism. IgE-stimulated Ca2+ influx was decreased by hydrocortisone pretreatment. Apparently, glucocorticoids specifically uncouple IgE-mediated Ca flux with subsequent inhibition of histamine and arachidonic acid release. Glucocorticoids are potent antiinflammatory agents effective in ameliorating the symptoms of immediate hypersensitivity and other allergic reactions.