Low susceptibility of NC/Nga mice to tumor necrosis factor-alpha-mediated lethality and hepatocellular damage with D-galactosamine sensitization

The susceptibility of NC/Nga mice to tumor necrosis factor (TNF)-alpha was examined by using sensitization with d-galactosamine (d-GalN). Administration of TNF-alpha and d-GalN killed none of the NC/Nga mice, whereas it killed all of the BALB/c mice. Treatment with TNF-alpha and d-GalN caused few he...

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Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 130(2009), 2 vom: 11. Feb., Seite 225-32
Auteur principal: Koide, Naoki (Auteur)
Autres auteurs: Morikawa, Akiko, Naiki, Yoshikazu, Tumurkhuu, Gantsetseg, Yoshida, Tomoaki, Ikeda, Hiroshi, Yokochi, Takashi
Format: Article en ligne
Langue:English
Publié: 2009
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't Antibodies, Monoclonal Antibodies, Monoclonal, Murine-Derived Fas protein, mouse NF-kappa B Recombinant Proteins Tumor Necrosis Factor-alpha anti-Fas monoclonal antibody fas Receptor plus... Galactosamine 7535-00-4 Caspase 3 EC 3.4.22.- Caspase 8
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Résumé:The susceptibility of NC/Nga mice to tumor necrosis factor (TNF)-alpha was examined by using sensitization with d-galactosamine (d-GalN). Administration of TNF-alpha and d-GalN killed none of the NC/Nga mice, whereas it killed all of the BALB/c mice. Treatment with TNF-alpha and d-GalN caused few hepatic lesions in NC/Nga mice but massive hepatocellular apoptosis in BALB/c mice. Unlike BALB/c mice, there was no elevation in caspase 3 and 8 activities in the livers of NC/Nga mice receiving TNF-alpha and d-GalN. On the other hand, administration of anti-Fas antibody definitely killed both NC/Nga and BALB/c mice via activation of caspases 3 and 8. Treatment with TNF-alpha and d-GalN led to translocation of nuclear factor (NF)-kappaB in NC/Nga and BALB/c mice. However, NF-kappaB translocation was sustained in NC/Nga mice, although it disappeared in BALB/c mice 7 h after the treatment. NF-kappaB inhibitors activated caspases 3 and 8, and enhanced TNF-alpha-mediated lethality in NC/Nga. Taken together, the low susceptibility of NC/Nga mice to TNF-alpha-mediated lethality was suggested to be responsible for the sustained NF-kappaB activation
Description:Date Completed 27.01.2009
Date Revised 10.12.2019
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2008.09.003