Source:http://linkedlifedata.com/resource/pubmed/id/17316614
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
2007-4-30
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| pubmed:abstractText |
The role of interleukin-18 (IL-18) in excitotoxic neurodegeneration is largely unknown. To address this issue, we used kainic acid (KA)-induced hippocampal neurodegeneration in IL-18 knockout (KO) mice. One day after KA administration, clinical symptoms and histopathological changes did not differ between IL-18 KO mice and wild-type mice. However, 7 days after KA application the hippocampal neurodegeneration was markedly severe in IL-18 KO mice as demonstrated by increased locomotion and prominent histopathological changes including neuronal cell loss, microglia activation and astrogliosis. Surprisingly, when wild-type mice received recombinant mouse IL-18 (rmIL-18) in advance, after KA treatment both the clinical and pathological signs were dose-dependently aggravated compared to mice without rmIL-18 pre-treatment. To clarify the mechanism behind this, we assessed the expression of the IL-18 associated cytokines IL-12, IL-1beta, interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) in the hippocampus by immunohistochemistry and flow cytometry. IL-12 and IFN-gamma expression was strongly increased in IL-18 KO mice when compared to wild-type mice 7 days after KA treatment in agreement with increased microglia activation. These results suggest that the role of IL-18 in excitotoxic injury in IL-18 deficient mice may be overcompensated by increased IL-12 secretion.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/Kainic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
0014-4886
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
205
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
64-73
|
| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:17316614-Adaptation, Physiological,
pubmed-meshheading:17316614-Animals,
pubmed-meshheading:17316614-Astrocytes,
pubmed-meshheading:17316614-Female,
pubmed-meshheading:17316614-Gliosis,
pubmed-meshheading:17316614-Hippocampus,
pubmed-meshheading:17316614-Interferon-gamma,
pubmed-meshheading:17316614-Interleukin-12,
pubmed-meshheading:17316614-Interleukin-18,
pubmed-meshheading:17316614-Kainic Acid,
pubmed-meshheading:17316614-Male,
pubmed-meshheading:17316614-Mice,
pubmed-meshheading:17316614-Mice, Inbred C57BL,
pubmed-meshheading:17316614-Mice, Knockout,
pubmed-meshheading:17316614-Microglia,
pubmed-meshheading:17316614-Motor Activity,
pubmed-meshheading:17316614-Nerve Degeneration,
pubmed-meshheading:17316614-Recombinant Proteins,
pubmed-meshheading:17316614-Severity of Illness Index
|
| pubmed:year |
2007
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| pubmed:articleTitle |
IL-18 deficiency aggravates kainic acid-induced hippocampal neurodegeneration in C57BL/6 mice due to an overcompensation by IL-12.
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| pubmed:affiliation |
Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Karolinska University Hospital in Huddinge, Stockholm, Sweden.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|