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Am J Physiol Lung Cell Mol Physiol (January 16, 2004). doi:10.1152/ajplung.00125.2003
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Submitted on April 28, 2003
Accepted on January 4, 2004

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

Nico A. Maris1*, Koenraad F. van der Sluijs1, Sandrine Florquin2, Alex F. de Vos1, Jennie M. Pater1, Henk M. Jansen3, and Tom van der Poll4

1 Department of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
2 Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
3 Department of Pulmonology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
4 Department of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Department of Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

* To whom correspondence should be addressed. E-mail: n.a.maris{at}amc.uva.nl.

Lipopolysaccharide is ubiquitously present in the environment. To determine the effect of salmeterol, a long acting {beta}2-receptor agonist, on lipopolysaccharide- induced lung inflammation, mice received lipopolysaccharide (10 µg) intranasally with or without salmeterol intraperitoneally (5 mg/kg) 30 minutes earlier and 12 hours 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, mice intranasally exposed to lipopolysaccharide were treated 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.




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