ArticleLiver international : official journal of the International Association for the Study of the Liver2011
Chronic alcohol-induced liver disease inhibits dendritic cell function.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- New insights in the pathogenesis of alcohol-related liver disease: The metabolic, immunologic, and neurologic pathwaysLiver research (Beijing, China) · 2023Review
- Role of alcohol in pathogenesis of hepatitis B virus infection.World journal of gastroenterology · 2020Review
- Abnormal Innate Immunity in Acute-on-Chronic Liver Failure: Immunotargets for Therapeutics.Frontiers in immunology · 2020Review
- Recent Insights Into the Role of Immune Cells in Alcoholic Liver Disease.Frontiers in immunology · 2019Review
- Chronic Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis via Immune Disturbances.Scientific reports · 2017Article
- Immunity and inflammatory signaling in alcoholic liver disease.Hepatology international · 2014Article
- Chronic ethanol diet increases regulatory T-cell activity and inhibits hepatitis C virus core-specific cellular immune responses in mice.Hepatology research : the official journal of the Japan Society of Hepatology · 2014Article
- Ethanol inhibits antigen presentation by dendritic cells.Clinical and vaccine immunology : CVI · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsWe have compared dendritic cell (DC) function derived from the alcoholic liver disease (ALD) sensitive Long-Evans (LE) and resistant Fischer rat strains to determine if the influence of ethanol on DCs was dependent on ALD.
methodsThe LE and Fischer rats were fed an ethanol-containing or isocaloric control liquid diet for 8 weeks and comparisons were made to LE rats injected with thioacetamide as a liver disease control. DCs were isolated from the spleen after expansion with human Fms-like tyrosine kinase receptor 3 ligand plasmid. Maturation markers CD86, CD80, CD40 and MHC-II were analysed by flow cytometry with or without lipopolysaccharide and poly I:C stimulation. Production of tumour necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin (IL)-12p40 and IL-10 cytokines and the antigen presentation ability of DCs was determined.
resultsOnly LE rats developed ALD characterized by liver injury, elevated alanine aminotransferase levels and steatosis; CD86 and CD40 expression was decreased in LE but not Fischer rats. Reduced TNF-α, IFN-γ, IL-12, proinflammatory and enhanced IL-10 cytokine production was found in DCs isolated from ethanol-fed LE but not Fischer rats. Allostimulatory activity was reduced in LE compared with the Fischer strain. In contrast, DCs isolated from thioacetamide-induced liver damage displayed a reduction only in IL-12p40; TNF-α, IL-10 and IFN-α production as well as antigen presenting ability remained intact compared with controls.
conclusionsALD sensitive LE rats exhibited characteristics of a suppressed DC phenotype that was not observed following thioacetamide-induced liver disease, which suggests an important role for ALD in altering the host cellular and humoral immune responses.
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Registered trials
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