Inhibition by fenoterol of human eosinophil functions including β 2 ‐adrenoceptor‐independent actions

Summary Agonists at β 2 adrenoceptors are used widely as bronchodilators in treating bronchial asthma. These agents also may have important anti‐inflammatory effects on eosinophils in asthma. We examined whether widely prescribed β 2 ‐adrenoceptor agonists differ in ability to suppress stimulus‐induced eosinophil effector functions such as superoxide anion (O 2 – ) generation and degranulation. To examine involvement of cellular adhesion in such responses, we also investigated effects of β 2 agonists on cellular adhesion and on CD11b expression by human eosinophils. O 2 – was measured using chemiluminescence. Eosinophil degranulation and adhesion were assessed by a radioimmunoassay for eosinophil protein X (EPX). CD11b expression was measured by flow cytometry. Fenoterol inhibited platelet‐activating factor (PAF)‐induced O 2 – generation by eosinophils significantly more than salbutamol or procaterol. Fenoterol partially inhibited PAF‐induced degranulation by eosinophils similarly to salbutamol or procaterol. Fenoterol inhibited phorbol myristate acetate (PMA)‐induced O 2 – generation and degranulation by eosinophils, while salbutamol or procaterol did not. Fenoterol inhibition of PMA‐induced O 2 – generation was not reversed by ICI‐118551, a selective β 2 ‐adrenoceptor antagonist. Fenoterol, but not salbutamol or procaterol, significantly inhibited PAF‐induced eosinophil adhesion. Fenoterol inhibited O 2 – generation and degranulation more effectively than salbutamol or procaterol; these effects may include a component involving cellular adhesion. Inhibition also might include a component not mediated via β 2 adrenoceptors.