Salmeterol, a 2-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice

Maris, Nico A., Koenraad F. van der Sluijs, Sandrine Florquin, Alex F. de Vos, Jennie M. Pater, Henk M. Jansen, and Tom van der Poll. Salmeterol, a 2-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice. Am J Physiol Lung Cell Mol Physiol 286: L1122–L1128, 2004. First published January 16, 2004; 10.1152/ajplung.00125.2003.—Lipopolysaccharide is ubiquitously present in the environment. To determine the effect of salmeterol, a long-acting 2-receptor agonist, on lipopolysaccharide-induced lung inflammation, mice received lipopolysaccharide (10 g) intranasally with or without salmeterol intraperitoneally (5 mg/kg) 30 min earlier and 12 h thereafter. Salmeterol doseand time-dependently inhibited the lipopolysaccharide-induced influx of neutrophils into bronchoalveolar lavage fluid and lung tissue, and these pulmonary neutrophils displayed a reduced expression of CD11b at their surface. To determine the contribution of the salmeterol effect on neutrophil CD11b in the attenuated neutrophil recruitment, we treated mice intranasally exposed to lipopolysaccharide with salmeterol with or without a blocking anti-CD11b antibody. Anti-CD11b profoundly reduced lipopolysaccharide-induced neutrophil influx in bronchoalveolar lavage fluid, an effect that was modestly enhanced by concurrent salmeterol treatment. These data suggest that salmeterol inhibits lipopolysaccharide-induced neutrophil recruitment to the lungs by a mechanism that possibly in part is mediated by an effect on neutrophil CD11b.