β2-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

AbstractPatients with chronic obstructive lung disorders often show increased susceptibility to airway infections. As β2-adrenoceptor agonists, in addition to reversing the contractile response of bronchial smooth muscles, may inhibit a variety of inflammatory and immuno-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 β2-adrenoceptor agonist, could modify human blood neutrophil recruitment and antimicrobial activity.Pre-exposure to fenoterol significantly reduced neutrophil migration towards the complement component C5a, at concentrations ranging from 10−7m to 10−5m , or towards lipopolysaccharide, at a concentration of 10−5m (P<0·05, each comparison). In contrast, the drug (10−8–10−5m) did not significantly modify the increased expression of lymphocyte function-associated antigen (LFA-1, i.e. CD11a/CD18) the macrophage antigen-1 (Mac-1, i.e. CD11b/CD18) induced by N -formylmethionylleucylphenylalanine (fMLP) (P>0·05, each comparison). Finally, incubation of neutrophils with fenoterol (10−8–10−5m) did not significantly influence phagocytosis or intracellular killing of bacteria (Staphylococcus aureus) or H2O2release induced by tetradecanoyl-phorbol-acetate (P>0·1 for each comparison).These results suggest that short-acting β2-adrenoceptor agonists, such as fenoterol, are able partially to reduce neutrophil recruitment in the airways without interfering with the processes involved in phagocytic activity against bacteria