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

M. Silvestri, S. Oddera, S. Lantero, G. A. Rossi

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Abstract

Patients 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 vivo whether fenoterol, a short-acting a-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 10-7 M to 10-5 M or towards lipopolysaccharide, at a concentration of 10-5 (P <0.05. each comparison). In contrast, the drug (10-8-10-5 M) 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 (10-8-10-5 M) did not significantly influence phagocytosis or intracellular killing of bacteria (Staphylococcus aureus) or H2O2 release 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.

Original languageEnglish
Pages (from-to)416-423
Number of pages8
JournalRespiratory Medicine
Volume93
Issue number6
DOIs
Publication statusPublished - 1999

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ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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