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Home ยป Sustained lipopolysaccharide-induced lung inflammation in mice is attenuated by functional deficiency of the Fas/Fas ligand system.

Sustained lipopolysaccharide-induced lung inflammation in mice is attenuated by functional deficiency of the Fas/Fas ligand system.

TitleSustained lipopolysaccharide-induced lung inflammation in mice is attenuated by functional deficiency of the Fas/Fas ligand system.
Publication TypeJournal Article
Year of Publication2004
AuthorsMatute-Bello, G, Winn, RK, Martin, TR, W Liles, C
JournalClin Diagn Lab Immunol
Volume11
Issue2
Pagination358-61
Date Published2004 Mar
ISSN1071-412X
KeywordsAdministration, Intranasal, Animals, Antigens, CD95, Bronchoalveolar Lavage Fluid, Fas Ligand Protein, Lipopolysaccharides, Male, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Pneumonia
Abstract

To determine whether the Fas/Fas ligand (FasL) (CD95/CD178) system contributes to the development of an inflammatory response in vivo, 2.5 microg 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.
Alternate JournalClin. Diagn. Lab. Immunol.
PubMed ID15013988