Title

Acute ethanol consumption synergizes with trauma to increase monocyte tumor necrosis factor alpha production late postinjury

UMMS Affiliation

Department of Medicine, Division of Gastroenterology; Department of Medicine, Rheumatology Division; Department of Surgery

Date

11-1-1994

Document Type

Article

Medical Subject Headings

Adult; Aged; Alcohol Drinking; Blotting, Northern; Female; Humans; Immune Tolerance; Macrophages; Male; Middle Aged; Sepsis; Transforming Growth Factor beta; Tumor Necrosis Factor-alpha; Wounds and Injuries

Disciplines

Digestive System Diseases | Gastroenterology

Abstract

The hypothesis that acute ethanol uptake plus trauma can synergize to increase immunosuppression was tested. We found that, unlike non-alcohol-exposed patients, patients with acute alcohol use prior to trauma have a transient decrease in monocyte tumor necrosis factor alpha (TNF alpha) production during the very early postinjury (0-3 days) period. However, TNF alpha production by these alcohol-exposed patients' monocytes (M0) became hyperelevated late postinjury (> 9 days). Consequently, these massively elevated M0 TNF alpha levels can contribute to posttrauma immunosuppression after acute alcohol use. We also demonstrate that normal monocyte activation with the superantigen, Staphylococcus enterotoxin B (SEB), results in a preferential induction of cell-associated M0 TNF alpha production, described as characteristic of immunosuppressed trauma patients. Acute in vitro ethanol treatment down-regulated the elevated TNF alpha production by trauma patients' M0 after either SEB, muramyl-dipeptide (MDP), interferon-gamma plus MDP, or lipopolysaccharide (LPS) stimulation. Both SEB- and LPS-induced TNF alpha mRNA induction was inhibited by acute alcohol treatment in normal M0, indicating that ethanol can regulate cytokine gene expression. An additional immunosuppressive effect of acute ethanol's stimulation was suggested by its induction of elevated transforming growth factor beta production in trauma patients' activated M0.

Rights and Permissions

Citation: J Clin Immunol. 1994 Nov;14(6):340-52.

Related Resources

Link to Article in PubMed

PubMed ID

7883861