Source:http://linkedlifedata.com/resource/pubmed/id/16039549
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001758,
umls-concept:C0022714,
umls-concept:C0023810,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0031809,
umls-concept:C0041904,
umls-concept:C0162493,
umls-concept:C0175697,
umls-concept:C0205245,
umls-concept:C0597357,
umls-concept:C0687080,
umls-concept:C1456820,
umls-concept:C1880177,
umls-concept:C2697656
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pubmed:issue |
11
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pubmed:dateCreated |
2005-7-25
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pubmed:abstractText |
It has been widely demonstrated that LPS is able to induce kinin B(1) receptor up-regulation throughout several models of inflammation. Using an in-vivo system in which LPS was administered systemically, we assessed the participation of the pro-inflammatory cytokine TNFalpha in the functional up-regulation of B(1) receptors in the mouse paw. Systemic treatment with LPS (10 microg/animal, i.v. 24 h before) resulted in a marked increase (about 5-fold) in the mouse paw edema induced by the selective B(1) receptor agonist des-Arg(9)-BK (50 nmol/paw) in both Swiss and C57/BL6 mice. The up-regulation of des-Arg(9)-BK-caused edema following LPS treatment was found to be greatly diminished in TNFalpha p55(-/-) receptor knockout mice. In addition, the paw edema evoked by des-Arg(9)-BK was significantly reduced when mice received the anti-TNFalpha antibody (100 [corrected] microg/kg, i.v.) 5 min before the LPS treatment. A similar inhibition of B(1) receptor-mediated paw edema was observed when mice were treated with thalidomide (30 mg/kg, s.c.) [corrected] a drug known for reducing TNFalpha synthesis, 5 min prior to LPS administration. ELISA experiment [corrected] revealed that TNFalpha serum levels were maximal at 1 h following LPS systemic treatment. Taken together, the present results suggest that the early production of the pro-inflammatory cytokine TNFalpha is probably responsible for driving the sequence of events involved in the functional up-regulation of B(1) receptors in the mouse paw.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Bradykinin,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Bradykinin B1,
http://linkedlifedata.com/resource/pubmed/chemical/Thalidomide,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/bradykinin, des-Arg(9)-
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1567-5769
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1593-600
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16039549-Animals,
pubmed-meshheading:16039549-Bradykinin,
pubmed-meshheading:16039549-Edema,
pubmed-meshheading:16039549-Inflammation,
pubmed-meshheading:16039549-Lipopolysaccharides,
pubmed-meshheading:16039549-Male,
pubmed-meshheading:16039549-Mice,
pubmed-meshheading:16039549-Mice, Inbred C57BL,
pubmed-meshheading:16039549-Mice, Knockout,
pubmed-meshheading:16039549-Receptor, Bradykinin B1,
pubmed-meshheading:16039549-Thalidomide,
pubmed-meshheading:16039549-Time Factors,
pubmed-meshheading:16039549-Tumor Necrosis Factor-alpha,
pubmed-meshheading:16039549-Up-Regulation
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pubmed:year |
2005
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pubmed:articleTitle |
Assessment of TNFalpha contribution to the functional up-regulation of kinin B(1) receptors in the mouse paw after treatment with LPS.
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pubmed:affiliation |
Department of Pharmacology, Center of Biological Sciences, Universidade Federal de Santa Catarina, Campus Universitário, 88049-900, Florianópolis, SC, Brazil.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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