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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2005-4-7
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pubmed:abstractText |
Most pathologies of the brain have an inflammatory component, associated with the release of cytokines such as interleukin-1beta (IL-1beta) from resident and infiltrating cells. The IL-1 type I receptor (IL-1RI) initiates a signalling cascade but the type II receptor (IL-1RII) acts as a decoy receptor. Here we have investigated the expression of IL-1beta, IL-1RI and IL-1RII in distinct inflammatory lesions in the rat brain. IL-1beta was injected into the brain to generate an inflammatory lesion in the absence of neuronal cell death whereas neuronal death was specifically induced by the microinjection of N-methyl-D-aspartate (NMDA). Using TaqMan RT-PCR and ELISA, we observed elevated de novo IL-1beta synthesis 2 h after the intracerebral microinjection of IL-1beta; this de novo IL-1beta remained elevated 24 h later. There was a concomitant increase in IL-1RI mRNA but a much greater increase in IL-1RII mRNA. Immunostaining revealed that IL-1RII was expressed on brain endothelial cells and on infiltrating neutrophils. In contrast, although IL-1beta and IL-1RI were elevated to similar levels in response to NMDA challenge, the response was delayed and IL-1RII mRNA expression was unchanged. The lesion-specific expression of IL-1 receptors suggests that the receptors are differentially regulated in a manner not directly related to the endogenous level of IL-1 in the CNS.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/N-Methylaspartate,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1 Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1 Type II
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0953-816X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1205-14
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pubmed:dateRevised |
2006-11-20
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pubmed:meshHeading |
pubmed-meshheading:15813930-Animals,
pubmed-meshheading:15813930-Blotting, Western,
pubmed-meshheading:15813930-Chemokines, CXC,
pubmed-meshheading:15813930-Encephalitis,
pubmed-meshheading:15813930-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:15813930-Gene Expression Regulation,
pubmed-meshheading:15813930-Immunohistochemistry,
pubmed-meshheading:15813930-Immunoprecipitation,
pubmed-meshheading:15813930-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:15813930-Interleukin-1,
pubmed-meshheading:15813930-Male,
pubmed-meshheading:15813930-N-Methylaspartate,
pubmed-meshheading:15813930-RNA, Messenger,
pubmed-meshheading:15813930-Rats,
pubmed-meshheading:15813930-Rats, Wistar,
pubmed-meshheading:15813930-Receptors, Interleukin-1,
pubmed-meshheading:15813930-Receptors, Interleukin-1 Type I,
pubmed-meshheading:15813930-Receptors, Interleukin-1 Type II,
pubmed-meshheading:15813930-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15813930-Statistics, Nonparametric,
pubmed-meshheading:15813930-Time Factors
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pubmed:year |
2005
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pubmed:articleTitle |
Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation.
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pubmed:affiliation |
Molecular Neuropathology Laboratory, School of Biological Sciences, University of Southampton, UK. docagne@cajal.csic.es
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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