Linked Life Data

10484462

Source:http://linkedlifedata.com/resource/pubmed/id/10484462

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 1
pubmed:dateCreated
1999-10-28
pubmed:abstractText
Acrolein is an environmental pollutant that is known to suppress respiratory host defense against infections; however, the mechanism of the decrease in host defense is not yet clear. We have previously reported that acrolein inhibited endotoxin-induced cytokine release and induced apoptosis in human alveolar macrophages, suggesting that the inhibition of cytokine release and/or cytotoxicity to alveolar macrophages may, in part, be responsible for acrolein-induced immunosuppression in the lung. Because nuclear factor-kappaB (NF-kappaB) is an important transcription factor for a number of cytokine genes and is also an important regulator of apoptosis, the effect of acrolein on NF-kappaB activity was examined by electrophoresis mobility shift assay. Acrolein caused a dose-dependent inhibition of endotoxin-induced NF-kappaB activation as well as an inhibition of basal level NF-kappaB activity. Because IkappaB is a principal regulator of NF-kappaB activity in the nucleus, changes in IkappaB were determined by Western blotting. Acrolein-inhibited IkappaB phosphorylation leads to an increase in cellular IkappaB levels preventing NF-kappaB nuclear translocation and is likely the mechanism of acrolein-induced inhibition of NF-kappaB activity. The role of basal level NF-kappaB in acrolein-induced apoptosis was also examined. An NF-kappaB inhibitor (MG-132) also induced apoptosis in human alveolar macrophages, suggesting that a certain basal level NF-kappaB activity may be required for macrophage cell survival. Taken together, our results suggest that the acrolein-inhibited endotoxin-induced NF-kappaB activation decreased the basal level NF-kappaB activity, which may be responsible for the inhibition of cytokine release and the induction of apoptosis in human alveolar macrophages.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L550-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Effect of acrolein on human alveolar macrophage NF-kappaB activity.
pubmed:affiliation
Toxicology Program, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Texas Houston Health Science Center, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.