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Ethanol‐induced inhibition of cytokine release and protein degranulation in human neutrophils
Author(s) -
Taïeb Julien,
Delarche Charlotte,
Ethuin Fréderic,
Selloum Saphia,
Poynard Thierry,
GougerotPocidalo MarieAnne,
CholletMartin Sylvie
Publication year - 2002
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.72.6.1142
Subject(s) - degranulation , cytokine , tumor necrosis factor alpha , biology , in vivo , in vitro , ethanol , hepatocyte growth factor , alcoholic liver disease , immune system , hepatocyte , liver injury , immunology , pharmacology , medicine , biochemistry , receptor , cirrhosis , microbiology and biotechnology
Ethanol impairs immune responses in humans and animal models, in vivo and in vitro. In particular, ethanol inhibits some key functions of human polymorphonuclear neutrophils (PMN). We investigated the impact of ethanol on cytokine production by highly purified PMN. In a time‐ and concentration‐dependent manner, ethanol inhibited the production of interleukin (IL)‐8 protein and mRNA and also hindered tumor necrosis factor α (TNF‐α) release by modulating the expression of the TNF‐α‐converting enzyme involved in TNF‐α shedding. This disruption of PMN cytokine release by ethanol may contribute to the increased risk of infection in alcoholic patients. Degranulation of hepatocyte growth factor (HGF) was also impaired by a clinically relevant ethanol concentration (0.8%), an action that may delay the repair of alcoholic liver damage. These findings suggest that ethanol may modulate three major cytokines involved in alcoholic liver diseases, IL‐8, TNF‐α, and HGF, via three different mechanisms.