Alcohol suppresses lipopolysaccharide-induced tumor necrosis factor activity in serum and lung.
Ethanol intoxication has been shown to suppress selected functions of the immune system thereby compromising host defense against bacterial infections. Tumor necrosis factor, a secretory protein produced by the macrophage in response to lipopolysaccharide, mediates the inflammatory cascade and stimulates phagocyte functions. Acute ethanol intoxication markedly suppressed both serum and lung tumor necrosis factor elicited in response to lipopolysaccharide. Furthermore, ethanol inhibited intratracheal lipopolysaccharide-induced neutrophil recruitment into the alveoli and prevented the fall in circulating neutrophils in response to intravenous lipopolysaccharide. Thus, the anti-inflammatory effects of ethanol may be secondary to suppression of macrophage-derived tumor necrosis factor.
Nelson
S
S
Department of Pulmonary/Critical Care Medicine, Louisiana State University Medical Center, New Orleans.
Bagby
G
G
Summer
W R
WR
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002452:Cell Count; D004926:Escherichia coli; D000431:Ethanol / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects / Q000378:metabolism*; D008264:Macrophages / Q000166:cytology; D008297:Male; D009504:Neutrophils / Q000166:cytology; D011650:Pulmonary Alveoli / Q000166:cytology; D051381:Rats; D011919:Rats, Inbred Strains; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D000431:Ethanol