REGULATION OF IGE PRODUCTION FROM HUMAN MONONUCLEAR-CELLS BY BETA-2-ADRENOCEPTOR AGONISTS

The present study examined the effect of beta 2-adrenoceptor agonists on the interleukin-4 (IL-4)-driven IgE production and on the possible mechanisms of action of these compounds. We present evidence that salb utamol and fenoterol potentiated the IL-4-induced IgE production by hu man peripheral blood mononuclear cells (PBMC). No significant effect o f incubation in the presence of beta 2-adrenoceptor agonists on IgG, I gA and IgM production was observed. Salbutamol and fenoterol inhibited interferon(IFN)-gamma production by PHA-activated human PBMC suggesti ng that the blockade of the production of this cytokine could possibly explain the enhancement of IgE production. Salbutamol and fenoterol p otentiated the IL-4-induced production of sCD23 whereas no effect on C D23 expression was observed. The potentiating effect of salbutamol on IgE production was blocked by two antagonists of beta 2-adrenoceptor, namely butoxamine and D,L-propranolol, suggesting a beta-adrenoceptor- mediated event. These results demonstrate that beta 2-adrenoceptor sti mulation results in an increase in IgE production by human B lymphocyt es.