Source:http://linkedlifedata.com/resource/pubmed/id/12122053
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
14
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| pubmed:dateCreated |
2002-7-17
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| pubmed:abstractText |
Inflammation is a critical factor for development of hypoxic-ischemic (HI) brain injury. Interleukin-18 (IL-18) is a proinflammatory cytokine expressed in microglia and processed by caspase-1. Our aim was to characterize the expression of IL-18 and its receptor in relation to caspase-1 and IL-1beta after HI and to evaluate to what extent IL-18 contributes to HI brain injury. Seven-day-old rats were subjected to HI, and brain tissue was sampled at different time points (3 hr to 14 d) after insult. The mRNA for IL-18 and caspase-1 were analyzed with reverse transcriptase PCR, protein was analyzed by Western blot (IL-18, caspase-1) or ELISA (IL-1beta), and the regional distribution was assessed by immunohistochemistry. HI was also induced in C57BL/6 mice, and brain injury in IL-18-deficient animals was compared with that in wild-type animals. The expression of mRNA/protein for caspase-1 and IL-18 in brain homogenates increased progressively at 12 hr to 14 d after HI, whereas IL-1beta peaked at 8 hr. A widespread expression of caspase-1 and IL-18 protein in microglia was found in the HI hemisphere. The IL-18 receptor was expressed on neurons of the cerebral cortex and thalamus. IL-1beta was primarily found in microglia in the habenular nucleus of the thalamus. The infarct volume was reduced by 21% (p = 0.01), and the neuropathology score was significantly decreased in the cerebral cortex (-35%), hippocampus (-22%), striatum (-18%), and thalamus (-17%) in mice with IL-18 deficiency compared with wild-type mice. In conclusion, we found that IL-18 expression in microglia was markedly increased after HI and that IL-18 appears to be important for the development of HI brain injury.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Il18r1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18 Receptor alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-18
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
1529-2401
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
15
|
| pubmed:volume |
22
|
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
5910-9
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12122053-Animals,
pubmed-meshheading:12122053-Animals, Newborn,
pubmed-meshheading:12122053-Blotting, Western,
pubmed-meshheading:12122053-Brain,
pubmed-meshheading:12122053-Brain Chemistry,
pubmed-meshheading:12122053-Caspase 1,
pubmed-meshheading:12122053-Disease Models, Animal,
pubmed-meshheading:12122053-Disease Progression,
pubmed-meshheading:12122053-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:12122053-Female,
pubmed-meshheading:12122053-Hypoxia-Ischemia, Brain,
pubmed-meshheading:12122053-Immunohistochemistry,
pubmed-meshheading:12122053-Interleukin-1,
pubmed-meshheading:12122053-Interleukin-18,
pubmed-meshheading:12122053-Interleukin-18 Receptor alpha Subunit,
pubmed-meshheading:12122053-Male,
pubmed-meshheading:12122053-Mice,
pubmed-meshheading:12122053-Mice, Inbred C57BL,
pubmed-meshheading:12122053-Mice, Knockout,
pubmed-meshheading:12122053-Microglia,
pubmed-meshheading:12122053-Neurons,
pubmed-meshheading:12122053-RNA, Messenger,
pubmed-meshheading:12122053-Rats,
pubmed-meshheading:12122053-Rats, Wistar,
pubmed-meshheading:12122053-Receptors, Interleukin,
pubmed-meshheading:12122053-Receptors, Interleukin-18,
pubmed-meshheading:12122053-Reverse Transcriptase Polymerase Chain Reaction
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| pubmed:year |
2002
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| pubmed:articleTitle |
Interleukin-18 involvement in hypoxic-ischemic brain injury.
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| pubmed:affiliation |
Department of Physiology and Pharmacology, Perinatal Center, Göteborg University, 405 30 Göteborg, Sweden.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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