Source:http://linkedlifedata.com/resource/pubmed/id/10374717
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1999-7-21
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pubmed:abstractText |
Intracerebral (i.c.) inoculation of susceptible strains of mice with Theiler's murine encephalomyelitis virus (TMEV) results in immune-mediated demyelinating disease. Interleukin-1 receptors are expressed in the brain of mice, in particular in the hippocampus, and have been implicated in neuroimmunoendocrine interactions. In the present study we investigated the regulation of interleukin-1 receptors in the hippocampus of a susceptible (SJL/J) and a resistant (BALB/c) strain of mice infected with TMEV, at different time intervals of the disease. Our results show that interleukin-1 receptors in the hippocampus were decreased in TMEV-infected mice at early times post-infection (10 and 14 days p.i.). The reduction in interleukin-1 receptors only occurred in the susceptible strain of mice (SJL/J), whereas interleukin-1 binding in the hippocampus of TMEV-infected resistant mice (BALB/c) showed values similar to those in control animals. The TMEV-induced down-regulation of interleukin-1 receptors was secondary to a marked decrease in the affinity of the receptor (control: Kd = 10.5 pM; TMEV: Kd = 1.30 pM) accompanied by a decrease in receptor number (control: Bmax = 2.189 fmol/mg protein; TMEV: B max = 0.84 fmol/mg protein). We also investigated the effects of glucocorticoid treatment on the regulation of hippocampal interleukin-1 receptors of TMEV-infected mice. Dexamethasone treatment in the early phase (500 microg/kg or 1 mg/kg during days 5-10 p.i.) of the disease significantly reversed the deficits in hippocampal interleukin-1 receptors observed at 10 days p.i. in SJL/J mice, and suppressed neurological signs of demyelination. These results suggest that: (i) the reduction of interleukin-1 receptors may be a consequence, at least in part, of local production of interleukin-1 at early times during TMEV infection; (ii) interleukin-1 seems to be a critical factor for the susceptibility to TMEV-induced demyelination and (iii) the protective effect of dexamethasone appears to be related to its ability to reverse the reduction in interleukin-1 receptors during the early disease. These results suggest that interleukin-1 is a pivotal mediator in TMEV-induced demyelination.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0014-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
7
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pubmed:volume |
372
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
75-83
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10374717-Animals,
pubmed-meshheading:10374717-Anti-Inflammatory Agents,
pubmed-meshheading:10374717-Demyelinating Diseases,
pubmed-meshheading:10374717-Dexamethasone,
pubmed-meshheading:10374717-Female,
pubmed-meshheading:10374717-Hippocampus,
pubmed-meshheading:10374717-Male,
pubmed-meshheading:10374717-Mice,
pubmed-meshheading:10374717-Mice, Inbred BALB C,
pubmed-meshheading:10374717-Mice, Inbred Strains,
pubmed-meshheading:10374717-Poliomyelitis,
pubmed-meshheading:10374717-Receptors, Interleukin-1,
pubmed-meshheading:10374717-Species Specificity,
pubmed-meshheading:10374717-Theilovirus,
pubmed-meshheading:10374717-Time Factors
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pubmed:year |
1999
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pubmed:articleTitle |
Dexamethasone regulation of interleukin-1-receptors in the hippocampus of Theiler's virus-infected mice: effects on virus-mediated demyelination.
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pubmed:affiliation |
Department of Neural Plasticity, Cajal Institute, CSIC, Madrid, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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