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.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Administration, Intranasal
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Animals
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Bronchoalveolar Lavage Fluid / immunology
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Fas Ligand Protein
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Lipopolysaccharides / pharmacology
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Male
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Membrane Glycoproteins / genetics*
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Membrane Glycoproteins / immunology*
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Membrane Glycoproteins / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Mutant Strains
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Pneumonia / immunology*
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Pneumonia / pathology
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Pneumonia / physiopathology*
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fas Receptor / genetics*
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fas Receptor / immunology*
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fas Receptor / metabolism
Substances
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Fas Ligand Protein
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Fasl protein, mouse
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Lipopolysaccharides
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Membrane Glycoproteins
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fas Receptor