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Published online before print November 21, 2003
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,1,,,2
Departments of
* Cell Biology, Neurobiology and Anatomy and
Surgery,
Burn and Shock Trauma Institute, and
Alcohol Research Program, Loyola University Medical Center, Maywood, Illinois
2 Correspondence: Professor Departments of Cell Biology, Neurobiology and Anatomy and Surgery, Loyola University Medical Center, Building 110, Room 4237, 2160 South First Avenue, Maywood, IL 60153. E-mail: ekovacs{at}lumc.edu
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.
Key Words: lipopolysaccharide • inflammation • signal transduction • suppression
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