Dissection of the Intracellular Pathways in Hepatocytes Suggests a Role for Jun Kinase and IFN Regulatory Factor-1 in Con A-Induced Liver Failure
Con A administration results in dose-dependent immune-mediated liver injury. Cytokines are important to determine the outcome of liver failure in this model, and especially TNF-alpha and IFN-gamma directly contribute to hepatocyte damage. The intracellular pathways of these two cytokines, which even...
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Published in | The Journal of immunology (1950) Vol. 167; no. 1; pp. 514 - 523 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Am Assoc Immnol
01.07.2001
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Abstract | Con A administration results in dose-dependent immune-mediated liver injury. Cytokines are important to determine the outcome of liver failure in this model, and especially TNF-alpha and IFN-gamma directly contribute to hepatocyte damage. The intracellular pathways of these two cytokines, which eventually result in tissue destruction, are not well defined. Here we used anti-IFN-gamma Abs and adenoviral vectors that express molecules inhibiting distinct TNF-alpha-dependent pathways in hepatocytes to better understand the relevance of specific intracellular signaling cascades for Con A-induced liver failure. We show that activation of TNF-alpha- and IFN-gamma-dependent intracellular pathways occurs prior to the influx of immune-activated cells into the liver and that anti-TNF-alpha and anti-IFN-gamma neutralizing Abs cannot block infiltration of these cells. Blocking experiments with Abs and adenoviral vectors showed that NF-kappaB activation and the Fas-associated death domain protein/caspase 8 cascade in hepatocytes during Con A-induced liver failure have no impact on tissue injury. Additionally, STAT1 activation alone after Con A injection in liver cells does not result in liver damage. In contrast, IFN-gamma-dependent expression of IFN regulatory factor-1 and TNF-alpha-dependent activation of c-Jun N-terminal kinase in liver cells correlates with liver cell damage after Con A injection. Therefore, our experiments indicate that 11418690 |
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AbstractList | Abstract
Con A administration results in dose-dependent immune-mediated liver injury. Cytokines are important to determine the outcome of liver failure in this model, and especially TNF-α and IFN-γ directly contribute to hepatocyte damage. The intracellular pathways of these two cytokines, which eventually result in tissue destruction, are not well defined. Here we used anti-IFN-γ Abs and adenoviral vectors that express molecules inhibiting distinct TNF-α-dependent pathways in hepatocytes to better understand the relevance of specific intracellular signaling cascades for Con A-induced liver failure. We show that activation of TNF-α- and IFN-γ-dependent intracellular pathways occurs prior to the influx of immune-activated cells into the liver and that anti-TNF-α and anti-IFN-γ neutralizing Abs cannot block infiltration of these cells. Blocking experiments with Abs and adenoviral vectors showed that NF-κB activation and the Fas-associated death domain protein/caspase 8 cascade in hepatocytes during Con A-induced liver failure have no impact on tissue injury. Additionally, STAT1 activation alone after Con A injection in liver cells does not result in liver damage. In contrast, IFN-γ-dependent expression of IFN regulatory factor-1 and TNF-α-dependent activation of c-Jun N-terminal kinase in liver cells correlates with liver cell damage after Con A injection. Therefore, our experiments indicate that IFN regulatory factor-1 and the c-Jun N-terminal kinase pathway are involved in determining hepatocyte damage during Con A-induced liver failure and thus may provide new targets for therapeutic intervention. Con A administration results in dose-dependent immune-mediated liver injury. Cytokines are important to determine the outcome of liver failure in this model, and especially TNF-alpha and IFN-gamma directly contribute to hepatocyte damage. The intracellular pathways of these two cytokines, which eventually result in tissue destruction, are not well defined. Here we used anti-IFN-gamma Abs and adenoviral vectors that express molecules inhibiting distinct TNF-alpha-dependent pathways in hepatocytes to better understand the relevance of specific intracellular signaling cascades for Con A-induced liver failure. We show that activation of TNF-alpha- and IFN-gamma-dependent intracellular pathways occurs prior to the influx of immune-activated cells into the liver and that anti-TNF-alpha and anti-IFN-gamma neutralizing Abs cannot block infiltration of these cells. Blocking experiments with Abs and adenoviral vectors showed that NF-kappaB activation and the Fas-associated death domain protein/caspase 8 cascade in hepatocytes during Con A-induced liver failure have no impact on tissue injury. Additionally, STAT1 activation alone after Con A injection in liver cells does not result in liver damage. In contrast, IFN-gamma-dependent expression of IFN regulatory factor-1 and TNF-alpha-dependent activation of c-Jun N-terminal kinase in liver cells correlates with liver cell damage after Con A injection. Therefore, our experiments indicate that 11418690 Con A administration results in dose-dependent immune-mediated liver injury. Cytokines are important to determine the outcome of liver failure in this model, and especially TNF- alpha and IFN- gamma directly contribute to hepatocyte damage. The intracellular pathways of these two cytokines, which eventually result in tissue destruction, are not well defined. Here we used anti-IFN- gamma Abs and adenoviral vectors that express molecules inhibiting distinct TNF- alpha -dependent pathways in hepatocytes to better understand the relevance of specific intracellular signaling cascades for Con A-induced liver failure. We show that activation of TNF- alpha - and IFN- gamma -dependent intracellular pathways occurs prior to the influx of immune-activated cells into the liver and that anti-TNF- alpha and anti-IFN- gamma neutralizing Abs cannot block infiltration of these cells. Blocking experiments with Abs and adenoviral vectors showed that NF- Kappa B activation and the Fas-associated death domain protein/caspase 8 cascade in hepatocytes during Con A-induced liver failure have no impact on tissue injury. Additionally, STAT1 activation alone after Con A injection in liver cells does not result in liver damage. In contrast, IFN- gamma -dependent expression of IFN regulatory factor-1 and TNF- alpha -dependent activation of c-Jun N-terminal kinase in liver cells correlates with liver cell damage after Con A injection. Therefore, our experiments indicate that IFN regulatory factor-1 and the c-Jun N-terminal kinase pathway are involved in determining hepatocyte damage during Con A-induced liver failure and thus may provide new targets for therapeutic intervention. |
Author | Plumpe, Jorg Kubicka, Stefan Streetz, Konrad Sass, G Korber, Kerstin Fregien, Bastian Tiegs, Gisa Manns, Michael P Trautwein, Christian Bischoff, Stephan C |
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Snippet | Con A administration results in dose-dependent immune-mediated liver injury. Cytokines are important to determine the outcome of liver failure in this model,... Abstract Con A administration results in dose-dependent immune-mediated liver injury. Cytokines are important to determine the outcome of liver failure in this... |
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SubjectTerms | Adaptor Proteins, Signal Transducing Animals Carrier Proteins - metabolism CD4-Positive T-Lymphocytes - pathology Cell Movement - immunology concanavalin A Concanavalin A - administration & dosage Concanavalin A - pharmacology DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - metabolism DNA-Binding Proteins - physiology fas Receptor - metabolism Fas-Associated Death Domain Protein Hepatocytes - enzymology Hepatocytes - immunology Hepatocytes - metabolism Hepatocytes - pathology Humans Immune Sera - administration & dosage Injections, Intravenous Interferon Regulatory Factor-1 Interferon-gamma - antagonists & inhibitors Interferon-gamma - immunology Interferon-gamma - physiology Intracellular Fluid - enzymology Intracellular Fluid - immunology JNK Mitogen-Activated Protein Kinases JNK protein Leukocyte Common Antigens - biosynthesis Liver Failure - enzymology Liver Failure - immunology Liver Failure - pathology Liver Failure - prevention & control Male Mice Mice, Inbred BALB C Mitogen-Activated Protein Kinases - physiology NF-kappa B - metabolism Phosphoproteins - antagonists & inhibitors Phosphoproteins - metabolism Phosphoproteins - physiology Signal Transduction - immunology STAT1 Transcription Factor Trans-Activators - antagonists & inhibitors Trans-Activators - metabolism Tumor Cells, Cultured Tumor Necrosis Factor-alpha - pharmacology |
Title | Dissection of the Intracellular Pathways in Hepatocytes Suggests a Role for Jun Kinase and IFN Regulatory Factor-1 in Con A-Induced Liver Failure |
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