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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0021469,
umls-concept:C0021755,
umls-concept:C0023418,
umls-concept:C0026336,
umls-concept:C0030685,
umls-concept:C0035820,
umls-concept:C0391871,
umls-concept:C0591833,
umls-concept:C0680255,
umls-concept:C1261322,
umls-concept:C1283071,
umls-concept:C1456820,
umls-concept:C1515655,
umls-concept:C1521761,
umls-concept:C1963578
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pubmed:issue |
10
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pubmed:dateCreated |
1993-12-10
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pubmed:abstractText |
TNF, a primary mediator of the response to infection, can be injurious to the organism when present in excessive quantities. Circulating soluble TNF receptors (sTNFR) appear to represent a natural mechanism that protects against circulating TNF. Two soluble TNF receptors (sTNFR-P55 and sTNFR-P75) circulate in vivo and are up-regulated in response to endotoxin. In this study, we investigated the kinetics of LPS-induced sTNFR release and the role of the cytokines TNF, leukemia inhibiting factor, IFN-gamma, and IL-1 in this process. The results show that LPS injection results in a rapid increase in levels of both sTNFR. Although sTNFR-P55 decreases after a peak at 30 min, sTNFR-P75 levels show a peak after 4 to 8 h, after which they slowly diminish. Both human TNF and murine TNF are capable of increasing levels of both sTNFR. Blocking circulating TNF by administration of 3 different anti-TNF agents before LPS injection (mAb to murine TNF, sTNFR55-Fc or sTNFR75-Fc) results in a significant increase of sTNFR-P55 levels, whereas only both sTNFR-Fc constructs also significantly increase sTNFR-P75 levels. Although IL-1 receptor antagonist pretreatment before LPS has no effect on TNF or sTNFR levels, leukemia inhibiting factor pretreatment significantly increases sTNFR-P55 levels. Pretreatment with anti IFN-gamma mAb before LPS results in a significant reduction in TNF and sTNFR-P55 levels, but sTNFR-P75 levels are significantly increased. Our data show that both sTNFR can be up-regulated by LPS and TNF. The influence of TNF, leukemia inhibiting factor, IL-1, and IFN-gamma on the kinetics of LPS-induced circulating sTNFR is discussed in the context of the pathophysiology of LPS-induced disease.
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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/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/LIF protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Leukemia Inhibitory Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Lif protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
151
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5554-62
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8228246-Animals,
pubmed-meshheading:8228246-Female,
pubmed-meshheading:8228246-Growth Inhibitors,
pubmed-meshheading:8228246-Interferon-gamma,
pubmed-meshheading:8228246-Interleukin-1,
pubmed-meshheading:8228246-Interleukin-6,
pubmed-meshheading:8228246-Leukemia Inhibitory Factor,
pubmed-meshheading:8228246-Lipopolysaccharides,
pubmed-meshheading:8228246-Lymphokines,
pubmed-meshheading:8228246-Mice,
pubmed-meshheading:8228246-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:8228246-Tumor Necrosis Factor-alpha
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pubmed:year |
1993
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pubmed:articleTitle |
LPS-induced sTNF-receptor release in vivo in a murine model. Investigation of the role of tumor necrosis factor, IL-1, leukemia inhibiting factor, and IFN-gamma.
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pubmed:affiliation |
Department of Surgery, Faculty II, University of Limburg, Maastricht, The Netherlands.
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pubmed:publicationType |
Journal Article
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