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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0013081,
umls-concept:C0017262,
umls-concept:C0021753,
umls-concept:C0021760,
umls-concept:C0023767,
umls-concept:C0023810,
umls-concept:C0041904,
umls-concept:C0079459,
umls-concept:C0086418,
umls-concept:C0141826,
umls-concept:C0162493,
umls-concept:C0185117,
umls-concept:C0206190,
umls-concept:C0243071,
umls-concept:C0392673,
umls-concept:C1456820,
umls-concept:C1883254,
umls-concept:C1948023,
umls-concept:C2348042,
umls-concept:C2911684
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pubmed:issue |
1
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pubmed:dateCreated |
1994-7-13
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pubmed:abstractText |
Human peritoneal macrophages were exposed to increasing doses of LPS or a synthetic lipid A analogue (SDZ MRL 953) and production of the cytokines IL-1 beta, IL-6, TNF-alpha, and G-CSF was assessed at the protein and mRNA level. Cells were also prestimulated with low doses of LPS and SDZ MRL 953 to study their adaptation to a secondary challenge with high doses of LPS. The ability of macrophages to produce high levels of TNF-alpha and IL-6 after stimulation with LPS could be relieved almost completely by preincubating cells with low doses of LPS. Decreases of TNF-alpha and IL-6 production resulted from inhibition of gene transcription and/or changes in mRNA stability, as transcript levels of these cytokines were down-modulated by the process of LPS adaptation. Surprisingly, however, adapted cells were able to synthesize even larger quantities of G-CSF and IL-1 beta when exposed to a secondary LPS challenge. mRNA levels of the adapted cells remained unaltered for IL-1 beta, but were slightly increased for G-CSF as assessed by Northern blot analysis. High doses of the synthetic lipid A analogue SDZ MRL 953 were also able to adapt macrophages to a secondary LPS challenge by down-regulating TNF-alpha and IL-6 production, whereas priming secretion of G-CSF and IL-1 beta as well. We describe here the discordant adaptation of human peritoneal macrophages to a secondary LPS stimulus in vitro. These findings appear to have ramifications for the in vivo endotoxin response during inflammation and also Gram-negative septicemia.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte Colony-Stimulating...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipid A,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/SDZ MRL 953,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
153
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
287-99
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7515924-Dinoprostone,
pubmed-meshheading:7515924-Gene Expression,
pubmed-meshheading:7515924-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:7515924-Humans,
pubmed-meshheading:7515924-Interleukin-1,
pubmed-meshheading:7515924-Interleukin-6,
pubmed-meshheading:7515924-Lipid A,
pubmed-meshheading:7515924-Lipopolysaccharides,
pubmed-meshheading:7515924-Macrophages, Peritoneal,
pubmed-meshheading:7515924-RNA, Messenger,
pubmed-meshheading:7515924-Sepsis,
pubmed-meshheading:7515924-Transforming Growth Factor beta,
pubmed-meshheading:7515924-Tumor Necrosis Factor-alpha
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pubmed:year |
1994
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pubmed:articleTitle |
Discordant adaptation of human peritoneal macrophages to stimulation by lipopolysaccharide and the synthetic lipid A analogue SDZ MRL 953. Down-regulation of TNF-alpha and IL-6 is paralleled by an up-regulation of IL-1 beta and granulocyte colony-stimulating factor expression.
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pubmed:affiliation |
Department of Internal Medicine I, Freiburg University Medical Center, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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