Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1989-5-5
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
673-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Alcohol suppresses lipopolysaccharide-induced tumor necrosis factor activity in serum and lung.
pubmed:affiliation
Department of Pulmonary/Critical Care Medicine, Louisiana State University Medical Center, New Orleans.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.