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Acute ethanol exposure inhibits macrophage IL‐6 production: role of p38 and ERK1/2 MAPK
Author(s) -
Goral Joanna,
Choudhry Mashkoor A.,
Kovacs Elizabeth J.
Publication year - 2004
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.0703350
Subject(s) - p38 mitogen activated protein kinases , lipopolysaccharide , mapk/erk pathway , kinase , intracellular , macrophage , ethanol , biology , microbiology and biotechnology , mitogen activated protein kinase , signal transduction , pharmacology , in vitro , immunology , biochemistry
Acute ethanol consumption has been linked to an increase in infectious complications in trauma and burn patients. Ethanol modifies production of a variety of macrophage‐derived immunoregulatory mediators. Lipopolysaccharide (LPS), a potent stimulator of inflammatory responses in macrophages, activates several intracellular signaling pathways, including mitogen‐activated protein kinases (MAPK). In the current study, we investigated the effect of acute ethanol exposure on in vivo activation of p38 and extracellularly regulated kinases 1 and 2 (ERK1/2) MAPK in murine macrophages and the corresponding, LPS‐stimulated interleukin (IL)‐6 production. We demonstrated that a single dose of ethanol transiently down‐regulated p38 and ERK1/2 activation levels (3–24 h after treatment) and impaired IL‐6 synthesis. Ethanol‐related reduction in IL‐6 production was not further affected by the presence of inhibitors of p38 and ERK1/2 (SB 202190 and PD 98059, respectively). These results demonstrate that acute ethanol exposure can impair macrophage IL‐6 production and indicate that this effect may result from ethanol‐induced alterations in intracellular signaling through p38 and ERK1/2.