Linked Life Data

2674560

Source:http://linkedlifedata.com/resource/pubmed/id/2674560

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-10-26
pubmed:abstractText
Since granulocyte-macrophage colony-stimulating factor (GM-CSF) has previously been shown to activate macrophages, it was of particular interest to study its effect on synthesis and release of tumor necrosis factor-alpha (TNF-alpha). GM-CSF alone was incapable of activating murine peritoneal macrophages to TNF-alpha release. However, in response to lipopolysaccharide (LPS), GM-CSF was found to prime macrophages for enhanced TNF-alpha production. This priming effect was short-lived and was superseded by the contrary, an unresponsiveness to LPS. The suppressed response was due to a delayed production of prostaglandin E2 (PGE2) which did not affect GM-CSF-enhanced TNF-alpha gene transcription but blocked TNF-alpha production. When PGE2 synthesis was inhibited by indomethacin, the priming effect of GM-CSF was entirely reconstituted. Thus, GM-CSF initially primes for TNF-alpha and subsequently for PGE2 release which, taken together, may represent an autoregulatory feed-back system that could restrict macrophage activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0277-6766
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
353-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Temporally different stimulation of TNF-alpha and PGE2 release from GM-CSF-primed macrophages.
pubmed:affiliation
Institute of Immunology, Philipps University, Marburg, FRG.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't