| pubmed-article:10484462 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10484462 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:10484462 | lifeskim:mentions | umls-concept:C0085236 | lld:lifeskim |
| pubmed-article:10484462 | lifeskim:mentions | umls-concept:C0001204 | lld:lifeskim |
| pubmed-article:10484462 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:10484462 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:10484462 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:10484462 | pubmed:issue | 3 Pt 1 | lld:pubmed |
| pubmed-article:10484462 | pubmed:dateCreated | 1999-10-28 | lld:pubmed |
| pubmed-article:10484462 | 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. | lld:pubmed |
| pubmed-article:10484462 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10484462 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10484462 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10484462 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10484462 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10484462 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10484462 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10484462 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10484462 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10484462 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:10484462 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:10484462 | pubmed:author | pubmed-author:HolianAA | lld:pubmed |
| pubmed-article:10484462 | pubmed:author | pubmed-author:LORR | lld:pubmed |
| pubmed-article:10484462 | pubmed:author | pubmed-author:HamiltonR... | lld:pubmed |
| pubmed-article:10484462 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10484462 | pubmed:volume | 277 | lld:pubmed |
| pubmed-article:10484462 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10484462 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10484462 | pubmed:pagination | L550-7 | lld:pubmed |
| pubmed-article:10484462 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:meshHeading | pubmed-meshheading:10484462... | lld:pubmed |
| pubmed-article:10484462 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10484462 | pubmed:articleTitle | Effect of acrolein on human alveolar macrophage NF-kappaB activity. | lld:pubmed |
| pubmed-article:10484462 | 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. | lld:pubmed |
| pubmed-article:10484462 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10484462 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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