Regulation of IgE production from human mononuclear cells by β2‐adrenoceptor agonists

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Abstract
Summary: The present study examined the effect of β2‐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 salbutamol and fenoterol potentiated the IL‐4‐induced IgE production by human peripheral blood mononuclear cells (PBMC). No significant effect of incubation in the presence of β2‐adrenoceptor agonists on IgG, IgA and IgM production was observed. Salbutamol and fenoterol inhibited interferon‐(IFN)‐γ production by PHA‐activated human PBMC suggesting that the blockade of the production of this cytokine could possibly explain the enhancement of IgE production. Salbutamol and fenoterol potentiated the IL‐4‐induced production of sCD23 whereas no effect on CD23 expression was observed. The potentiating effect of salbutamol on IgE production was blocked by two antagonists of β2‐adrenoceptor, namely butoxamine and D,L‐propranolol, suggesting a β‐adrenoceptor‐mediated event. These results demonstrate that β2‐adrenoceptor stimulation results in an increase in IgE production by human B lymphocytes.