Linked Life Data

11770040

Source:http://linkedlifedata.com/resource/pubmed/id/11770040

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-12-24
pubmed:abstractText
During septic shock, circulating levels of anti-inflammatory mediators are increased relative to those of pro-inflammatory. The reduced capacity of septic shock blood leukocytes in expressing pro-inflammatory genes in response to bacterial lipopolysaccharide endotoxin (LPS) may contribute to reductions in these mediators, but the reasons for persistent increases in circulating anti-inflammatory mediators are unknown. We determined whether septic shock leukocytes that have adapted to LPS induction of the IL-1beta gene could continue to express sIL-1RA in response to LPS. Septic shock whole-blood leukocytes and neutrophils (PMNs) selectively maintained production of sIL-1RA after treatment with LPS while limiting that of IL-1beta. Repressed transcription of IL-1beta and rapid decay of IL-1beta mRNA in septic shock neutrophils correlated with reductions in levels of IL-1beta after stimulation with LPS. Transcription of sIL-1RA mRNA was also suppressed, but the ability of LPS to stimulate events that lead to efficient translation of a stable sIL-1RA mRNA appeared responsible for maintaining sIL-1RA production. We conclude that LPS adaptation of septic shock leukocytes selectively influences signaling pathways that regulate transcription, mRNA processing, and translation, leading to changes in the balance of production of pro- and anti-inflammatory mediators.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1073-2322
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
430-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11770040-Adaptation, Physiological, pubmed-meshheading:11770040-Anti-Inflammatory Agents, pubmed-meshheading:11770040-Case-Control Studies, pubmed-meshheading:11770040-Humans, pubmed-meshheading:11770040-Inflammation Mediators, pubmed-meshheading:11770040-Interleukin 1 Receptor Antagonist Protein, pubmed-meshheading:11770040-Interleukin-1, pubmed-meshheading:11770040-Leukocytes, pubmed-meshheading:11770040-Lipopolysaccharides, pubmed-meshheading:11770040-Models, Biological, pubmed-meshheading:11770040-Neutrophils, pubmed-meshheading:11770040-Protein Biosynthesis, pubmed-meshheading:11770040-RNA, Messenger, pubmed-meshheading:11770040-Shock, Septic, pubmed-meshheading:11770040-Sialoglycoproteins, pubmed-meshheading:11770040-Signal Transduction, pubmed-meshheading:11770040-Transcription, Genetic
pubmed:year
2001
pubmed:articleTitle
Endotoxin-adapted septic shock leukocytes selectively alter production of sIL-1RA and IL-1beta.
pubmed:affiliation
Section on Infectious Diseases, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27104, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.