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Clinical and Diagnostic Laboratory Immunology, March 2004, p. 358-361, Vol. 11, No. 2
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.2.358-361.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Sustained Lipopolysaccharide-Induced Lung Inflammation in Mice Is Attenuated by Functional Deficiency of the Fas/Fas Ligand System

Medical Research Service, VA Puget Sound Health Care System,¹ Divisions of Pulmonary and Critical Care Medicine,² Allergy and Infectious Diseases, Department of Medicine,⁴ Department of Surgery, University of Washington School of Medicine, Seattle, Washington³

Received 17 March 2003/ Returned for modification 31 October 2003/ Accepted 26 November 2003

To determine whether the Fas/Fas ligand (FasL) (CD95/CD178) system contributes to the development of an inflammatory response in vivo, 2.5 µg of bacterial lipopolysaccharide (LPS; endotoxin) per g was administered intranasally to healthy mice (C57BL/6) and mutant mice deficient in either Fas (lpr mice) or FasL (gld mice). Sustained LPS-induced neutrophilic inflammation in the lungs was attenuated in both lpr and gld mice. These observations provide further evidence of a proinflammatory role for the Fas/FasL system in the lungs.

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