Document Detail

Ethanol increases tumor necrosis factor-alpha receptor-1 (TNF-R1) levels in hepatic, intestinal, and cardiac cells.
MedLine Citation:
PMID:  15353169     Owner:  NLM     Status:  MEDLINE    
Chronic ethanol consumption leads to cell injury in virtually every tissue. Tumor necrosis factor-alpha (TNF-alpha) constitutes a major factor in the development of alcohol-induced liver injury. In alcohol-dependent subjects, elevated levels of plasma TNF-alpha are strongly predictive of mortality. Binding of TNF-alpha to TNF-alpha receptor-1 (TNF-R1) activates death domain pathways, leading to necrosis and apoptosis in most tissues, and it also increases the expression of intercellular adhesion molecules (i.e., ICAM-1), which promote inflammation. We determined whether ethanol exposure leads to increases in cellular TNF-R1. We incubated HepG2 human hepatoma cells and H4-II-E-C3 rat hepatoma cells with 25, 50, and 100 mM ethanol for various intervals of time up to 48 h. Human colonic adenocarcinoma cells (Caco-2 cells) and neonatal rat primary cardiomyocytes were also incubated with different concentrations of ethanol. Levels of TNF-R1 were measured either by a sandwich enzyme-linked immunosorbent assay (ELISA) method or by determining the extracellular transmembrane domain of TNF-R1 by an intact-cell ELISA method. Ethanol exposure for 48 h increased TNF-R1 levels in human hepatoma cells in a dose-dependent manner. Levels increased significantly by 164% at 50 mM and by 240% at 100 mM ethanol. Effects were time dependent and did not reach a plateau at 48 h. Similar increases in TNF-R1 were also observed in rat hepatoma cells (90% at 50 mM and 230% at 100 mM ethanol). Under similar conditions, Caco-2 cells showed a significant 80% increase in TNF-R1 levels at 200 mM ethanol, a concentration found in intestine. Neonatal rat primary cardiomyocytes showed TNF-R1 increases of 36% at 50 mM and 44% at 100 mM ethanol. These results indicate that exposure of different cell types to pharmacologic concentrations of ethanol increases TNF-R1 levels and may augment TNF-alpha-mediated cell injury in different tissues.
Diego A Rodriguez; Claudio Moncada; Marco T Núñez; Sergio Lavandero; Biddanda C Ponnappa; Yedy Israel
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Alcohol (Fayetteville, N.Y.)     Volume:  33     ISSN:  0741-8329     ISO Abbreviation:  Alcohol     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-09-08     Completed Date:  2005-02-11     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8502311     Medline TA:  Alcohol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  9-15     Citation Subset:  IM    
Millennium Institute for Advanced Studies in Cell Biology and Biotechnology, University of Chile, Santiago 6531057, Chile.
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MeSH Terms
Caco-2 Cells
Cell Line, Tumor
Cells, Cultured
Dose-Response Relationship, Drug
Ethanol / pharmacology*
Intestines / cytology,  drug effects*,  metabolism
Liver / cytology,  drug effects*,  metabolism
Myocytes, Cardiac / cytology,  drug effects*,  metabolism
Rats, Sprague-Dawley
Receptors, Tumor Necrosis Factor, Type I / biosynthesis*
Up-Regulation / drug effects*
Grant Support
Reg. No./Substance:
0/Receptors, Tumor Necrosis Factor, Type I; 64-17-5/Ethanol

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