beta(2)-agonist-induced inhibition of neutrophil chemotaxis is not associated with modification of LFA-1 and Mac-1 expression or with impairment of polymorphonuclear leukocyte antibacterial activity

Patients with chronic obstructive lung disorders often show increased susce ptibility to airway infections. As beta(2)-adrenoceptor agonists, in additi on to reversing the contractile response of bronchial smooth muscles, may i nhibit a variety of inflammatory and immune-effector cell functions, it is possible that these drugs interfere with host defence mechanisms. The present study was designed to test in vitro whether fenoterol, a short- acting beta(2)-adrenoceptor agonist, could modify human blood neutrophil re cruitment and antimicrobial activity. Pre-exposure to fenoterol significantly reduced neutrophil migration toward s the complement component C5a, at concentrations ranging from 10(-7) M to 10(-5) M, or towards lipopolysaccharide, at a concentration of 10(-5) M (P< 0.05, each comparison). In contrast, the drug (10(-8)-10(-5) M) did not sig nificantly modify the increased expression of lymphocyte function-associate d antigen (LFA-1, i.e. CD11a/CD18) the macrophage antigen-1 (Mac-1, i.e. CD 11b/CD18) induced by N-formylmethionylleucylphenylalanine (fMLP) (P>0.05, e ach comparison). Finally, incubation of neutrophils with fenoterol (10(-8)- 10(-5) M) did not significantly influence phagocytosis or intracellular kil ling of bacteria (Staphylococcus aureus) or H2O2 release induced by tetrade canoyl-phorbol-acetate (P>0.1 for each comparison). These results suggest that short-acting beta(2)-adrenoceptor agonists, such as fenoterol, are able partially to reduce neutrophil recruitment in the a irways without interfering with the processes involved in phagocytic activi ty against bacteria.