Contribution of TNF/TNF receptor and of Fas ligand to toxicity in murine models of endotoxemia and bacterial peritonitis
Détails
ID Serval
serval:BIB_821447C843A3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Contribution of TNF/TNF receptor and of Fas ligand to toxicity in murine models of endotoxemia and bacterial peritonitis
Périodique
Journal of Inflammation
ISSN
1078-7852
Statut éditorial
Publié
Date de publication
1995
Peer-reviewed
Oui
Volume
47
Numéro
4
Pages
173-9
Notes
Journal Article
Résumé
Fas/Fas ligand and TNF/TNF receptors are involved in apoptosis. Whether both systems are involved in septic shock has not been determined so far. We investigated the role of TNF/TNFR and Fas/Fas ligand in models of endotoxemia and of speticemia in mice. Upon LPS challenge, TNF and TNFR p55 were involved in the process inducing lethality. FasL did not contribute to enhance lethality, as evidenced in gld mice, lacing FasL. Following an intraperitoneal injection of live E. coli, TNF and TNFR p55 were necessary to combat infection. Disruption of either gene was associated with enhanced lethality and failure to clear the bacteria. No effect observed in gld mice in this peritonitis model. Thus, these observations confirmed the pathogenic role of TNF/TNFR in endotoxemia and its beneficial role in local bacterial infections. In addition the data ruled out a major role for Fas/FasL in septic shock in mice.
Mots-clé
Animals
Antigens, CD/physiology
Apoptosis
Disease Models, Animal
Endotoxins/toxicity
Escherichia coli Infections/*etiology/therapy
Fas Ligand Protein
Galactosamine/immunology
Lipopolysaccharides/toxicity
Lymphotoxin-alpha/physiology
Membrane Glycoproteins/*physiology
Mice
Mice, Inbred C57BL
Peritonitis/*etiology/therapy
Receptors, Tumor Necrosis Factor/physiology
Receptors, Tumor Necrosis Factor, Type I
Shock, Septic/etiology/therapy
Toxemia/*etiology/therapy
Tumor Necrosis Factor-alpha/antagonists & inhibitors/*physiology
Pubmed
Web of science
Création de la notice
21/01/2008 10:04
Dernière modification de la notice
20/08/2019 14:42