Cited by 179Alcohol Consumption and Health EffectsCell death mechanisms and regulationLiver physiology and pathology

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Elevated interleukin-6 during ethanol consumption acts as a potential endogenous protective cytokine against ethanol-induced apoptosis in the liver: involvement of induction of Bcl-2 and Bcl-xL proteins

Hong, Feng, Kim, Won-Ho, Tian, Zhigang, Jaruga, Barbara, Ishac, Edward, Shen, Xuening, Gao, Bin·2002·Oncogene

DOI 10.1038/sj.onc.1205016

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Abstract

Elevation of serum interleukin-6 (IL-6) levels is always associated with alcoholic liver disease (ALD), but the significance of such elevation is not clear. Here we show that chronic ethanol consumption induces significant apoptosis in the liver of IL-6 (-/-) mice but not IL-6 (+/+) mice. IL-6 (-/-) hepatocytes are more susceptible to ethanol- and tumor necrosis factor alpha- (TNFalpha-) induced apoptotic killing, which can be corrected by IL-6. Expression of both anti-apoptotic (such as Bcl-2 and Bcl-x(L)) and proapoptotic (such as Bax) proteins is markedly elevated in the liver of human ALD and chronically ethanol-fed IL-6 (+/+) mice. On the contrary, induction of Bcl-2 and Bcl-x(L) is not observed in the liver of chronically ethanol-fed IL-6 (-/-) mice, whereas expression of Bax protein remains elevated. Injection of IL-6 markedly induces expression of Bcl-2 and Bcl-x(L) but not Bax in the liver. Finally, high concentrations of ethanol inhibit IL-6-activated anti-apoptotic signal, but increasing the concentrations of IL-6 is able to overcome such inhibitory effect. These findings suggest that elevated serum IL-6 levels in ALD may overcome the inhibitory effect of ethanol on IL-6-mediated anti-apoptotic signals and prevent alcohol-induced hepatic apoptosis by induction of Bcl-2 and Bcl-x(L).

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Physiological potential of cytokines and liver damages
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Up-regulation of Siah1 by ethanol triggers apoptosis in neural crest cells through p38 MAPK-mediated activation of p53 signaling pathway
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Therapeutic potential of interleukin-6 in preventing obesity- and alcohol-associated fatty liver transplant failure
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Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice
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Bile acids inhibit interleukin-6 signaling via gp130 receptor-dependent and -independent pathways in rat liver
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Sulforaphane restores acetyl-histone H3 binding to Bcl-2 promoter and prevents apoptosis in ethanol-exposed neural crest cells and mouse embryos
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Authors: Hong, F., Kim, W.-H., Tian, Z., Jaruga, B., Ishac, E., Shen, X., & Gao, B.
Affiliations: National Institutes of Health (US)
University of Science and Technology of China (CN)
Virginia Commonwealth University (US)
Corresponding author: Gao, Bin
ORCID: Kim, Won-Ho
Tian, Zhigang
Gao, Bin
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2002-01-03
Volume: 21
Issue: 1
Pages: 32-43
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1205016
OpenAlex: W2057210516
Cited by: 179
References: 0
Citations by year: 2026: 2 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 4 · 2021: 8 · 2020: 10 · 2019: 7 · 2018: 7 · 2017: 10 · 2016: 8 · 2015: 6 · 2014: 6 · 2013: 7 · 2012: 11
FWCI: 7.68
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01aa012637-03)
National Institute on Alcohol Abuse and Alcoholism (R01 AA 12637)
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: interleukin-6, ethanol consumption, alcoholic liver disease, hepatocyte apoptosis, Bcl-2, Bcl-xL, Bax, TNF-α, anti-apoptotic signaling, IL-6 knockout mice
MeSH terms: Ethanol, Alcoholism, Animals, Body Weight, Cells, Cultured, Gene Expression Regulation, Genotype, Humans, Liver, Liver Diseases, Alcoholic, Male, Organ Size, Tumor Necrosis Factor-alpha, Interleukin-6, Apoptosis, Mice, Knockout, Proto-Oncogene Proteins c-bcl-2, Genes, bcl-2, Genetic Predisposition to Disease, Hepatocytes, bcl-X Protein, Mice

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Elevated interleukin-6 during ethanol consumption acts as a potential endogenous protective cytokine against ethanol-induced apoptosis in the liver: involvement of induction of Bcl-2 and Bcl-xL proteins

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