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Acute Lung Injury
2-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice
1Departments of Experimental Internal Medicine, 2Pathology, 3Pulmonology, and 4Infectious Diseases, Tropical Medicine & AIDS, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands
Submitted 28 April 2003 ; accepted in final form 4 January 2004
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 µg) intranasally with or without salmeterol intraperitoneally (5 mg/kg) 30 min earlier and 12 h thereafter. Salmeterol dose- and 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.
bronchodilator agents; neutrophils; endotoxins
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