Acute alcohol infusion suppresses endotoxin-induced serum tumor necrosis factor.
Tumor necrosis factor (TNF) is suggested to play an important role in host defense as well as in eliciting some of the metabolic alterations in endotoxemia. Bacteria and their products are involved in triggering the production and release of TNF. Alcohol consumption is known to suppress the immune system and increase susceptibility to infections. The present study was undertaken to investigate the effect of acute ethanol administration on the ability of endotoxin to increase circulating TNF levels and to determine the relationship between blood ethanol levels and endotoxin-induced serum TNF. A 50% decrease in serum TNF levels was seen 1-1.5 h after endotoxin challenge in conscious rats with blood alcohol levels between 75-175 mg/dl. A dose-related depression of serum TNF was observed with increasing blood alcohol levels. This was accompanied by a markedly diminished hyperlactacidemia seen following endotoxin administration. These data suggest that impaired TNF release may have a role in the altered immune response of alcoholics to infection.
D'Souza
N B
NB
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Bagby
G J
GJ
Nelson
S
S
Lang
C H
CH
Spitzer
J J
JJ
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D004731:Endotoxins / Q000037:antagonists & inhibitors*; D000431:Ethanol / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D007773:Lactates / Q000097:blood; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
D001786:Blood Glucose; D004731:Endotoxins; D007773:Lactates; D014409:Tumor Necrosis Factor-alpha; D000431:Ethanol