CD95/CD95 ligand interactions on epithelial cells in host defense to Pseudomonas aeruginosa

Science. 2000 Oct 20;290(5491):527-30. doi: 10.1126/science.290.5491.527.

Abstract

Pseudomonas aeruginosa causes severe infections, particularly of the lung, that are life threatening. Here, we show that P. aeruginosa infection induces apoptosis of lung epithelial cells by activation of the endogenous CD95/CD95 ligand system. Deficiency of CD95 or CD95 ligand on epithelial cells prevented apoptosis of lung epithelial cells in vivo as well as in vitro. The importance of CD95/CD95 ligand-mediated lung epithelial cell apoptosis was demonstrated by the rapid development of sepsis in CD95- or CD95 ligand-deficient mice, but not in normal mice, after P. aeruginosa infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Bone Marrow Transplantation
  • Cell Line
  • Epithelial Cells / immunology*
  • Epithelial Cells / microbiology
  • Epithelial Cells / pathology
  • Fas Ligand Protein
  • Humans
  • In Situ Nick-End Labeling
  • Lung / immunology*
  • Lung / microbiology
  • Lung / pathology
  • Lung Diseases / immunology*
  • Lung Diseases / microbiology
  • Lung Diseases / pathology
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism*
  • Mice
  • Mice, Inbred C3H
  • Pseudomonas Infections / immunology*
  • Pseudomonas Infections / microbiology
  • Pseudomonas Infections / pathology
  • Pseudomonas aeruginosa / immunology
  • Pseudomonas aeruginosa / pathogenicity*
  • Sepsis / microbiology
  • Spleen / microbiology
  • fas Receptor / genetics
  • fas Receptor / metabolism*

Substances

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