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

Clin Diagn Lab Immunol. 2004 Mar;11(2):358-61. doi: 10.1128/cdli.11.2.358-361.2004.


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

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Administration, Intranasal
  • Animals
  • Bronchoalveolar Lavage Fluid / immunology
  • Fas Ligand Protein
  • Lipopolysaccharides / pharmacology
  • Male
  • Membrane Glycoproteins / genetics*
  • Membrane Glycoproteins / immunology*
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Pneumonia / immunology*
  • Pneumonia / pathology
  • Pneumonia / physiopathology*
  • fas Receptor / genetics*
  • fas Receptor / immunology*
  • fas Receptor / metabolism


  • Fas Ligand Protein
  • Fasl protein, mouse
  • Lipopolysaccharides
  • Membrane Glycoproteins
  • fas Receptor