Source:http://linkedlifedata.com/resource/pubmed/id/18279308
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2008-2-18
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| pubmed:abstractText |
Interleukin-1 (IL-1) is one of the most important cytokines in neuroinflammation, in acute conditions as well as during natural ageing and neurodegenerative disorders. Using a transgenic mouse strain with brain-directed overexpression of IL-1 receptor antagonist (Tg hsIL-1ra), we show that blocking IL-1 receptor-mediated activity resulted in abolishing the alterations in neurogenesis in response to acute and chronic neuroinflammation. In addition, using a novel approach to quantifying glial activation, we show that expression of the astrocyte cytoskeletal marker glial fibrillary acidic protein (GFAP) following kainic acid (KA)-induced seizures or during ageing did not change in Tg hsIL-1ra animals. Nevertheless, the astrocyte morphology showed major alterations, consisting of fragmentation of the processes in Tg hsIL-1ra mice. Similarly, although there was a higher degree of basal microglial activation in the transgenic mice than wild-type animals, there was no change following KA-induced seizures or with ageing. Taken together, our results indicate that IL-1 is crucial for the adaptability of the brain to acute and chronic neuroinflammation.
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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 |
Feb
|
| pubmed:issn |
1460-9568
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
27
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
549-58
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| pubmed:meshHeading |
pubmed-meshheading:18279308-Adaptation, Physiological,
pubmed-meshheading:18279308-Aging,
pubmed-meshheading:18279308-Animals,
pubmed-meshheading:18279308-Astrocytes,
pubmed-meshheading:18279308-Cell Proliferation,
pubmed-meshheading:18279308-Encephalitis,
pubmed-meshheading:18279308-Glial Fibrillary Acidic Protein,
pubmed-meshheading:18279308-Gliosis,
pubmed-meshheading:18279308-Humans,
pubmed-meshheading:18279308-Interleukin 1 Receptor Antagonist Protein,
pubmed-meshheading:18279308-Interleukin-1,
pubmed-meshheading:18279308-Male,
pubmed-meshheading:18279308-Mice,
pubmed-meshheading:18279308-Mice, Knockout,
pubmed-meshheading:18279308-Mice, Transgenic,
pubmed-meshheading:18279308-Microglia,
pubmed-meshheading:18279308-Nerve Regeneration,
pubmed-meshheading:18279308-Neuronal Plasticity,
pubmed-meshheading:18279308-Neurons,
pubmed-meshheading:18279308-Seizures
|
| pubmed:year |
2008
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| pubmed:articleTitle |
Blunted neurogenesis and gliosis due to transgenic overexpression of human soluble IL-1ra in the mouse.
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| pubmed:affiliation |
Department of Neurobiology, Care Sciences and Society, Novum, floor 5, Division of Neurodegeneration and Neuroinflammation, Karolinska Institutet, SE-141 86 Stockholm, Sweden. stefan.spulber@ki.se
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|