Source:http://linkedlifedata.com/resource/pubmed/id/10859481
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-8-17
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pubmed:abstractText |
Interleukin (IL)-18 is a proinflammatory cytokine and a stimulator of cell-mediated immune responses. We have previously reported that acute stress stimulates the production of IL-18 mRNA in the glucocorticoid (GC)-producing cells of the adrenal cortex. In order to investigate the mechanisms governing the expression of IL-18 in the adrenal cortex, the effects of acute ACTH or chronic corticosterone treatment on the levels of IL-18 mRNA and protein were examined by in situ hybridization and Northern and Western blot assays. Adult male Sprague-Dawley rats received a subcutaneous injection of ACTH or subcutaneous implantation of slow-release corticosterone pellets followed by an injection of saline or ACTH. After 4 h, ACTH induced a 4-fold increase in IL-18 mRNA levels and elevated the content of pro-IL-18 peptide. Six days of chronic corticosterone treatment did not alter the basal levels of IL-18 mRNA and reduced those of pro-IL-18. Finally, ACTH treatment of animals under the corticosterone regimen induced a 2-fold increase in IL-18 mRNA and elevated the levels of the pro-IL-18 protein. The levels of the precursor, p45, and the active subunit p10 peptides of the IL-18-processing enzyme, IL-1beta-converting enzyme (ICE), showed no substantial differences in all the conditions tested. IL-1beta was not detected under these experimental conditions. These data demonstrate that the production of IL-18 in the adrenal cortex is stimulated by ACTH treatment and is not inhibited by the direct action of corticosterone. In contrast to the anti-inflammatory action of GCs, IL-18 may have an immunostimulatory role during acute stress.
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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:issn |
1021-7401
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2000 S. Karger AG, Basel
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pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10859481-Adrenal Cortex,
pubmed-meshheading:10859481-Adrenocorticotropic Hormone,
pubmed-meshheading:10859481-Animals,
pubmed-meshheading:10859481-Blotting, Northern,
pubmed-meshheading:10859481-Blotting, Western,
pubmed-meshheading:10859481-Corticosterone,
pubmed-meshheading:10859481-Gene Expression,
pubmed-meshheading:10859481-Hypothalamo-Hypophyseal System,
pubmed-meshheading:10859481-In Situ Hybridization,
pubmed-meshheading:10859481-Interleukin-18,
pubmed-meshheading:10859481-Male,
pubmed-meshheading:10859481-Pituitary-Adrenal System,
pubmed-meshheading:10859481-RNA, Messenger,
pubmed-meshheading:10859481-Rats,
pubmed-meshheading:10859481-Rats, Sprague-Dawley,
pubmed-meshheading:10859481-Stress, Physiological
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pubmed:year |
2000
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pubmed:articleTitle |
Modulation of IL-18 production in the adrenal cortex following acute ACTH or chronic corticosterone treatment.
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pubmed:affiliation |
Laboratory of Molecular Neurobiology, Weill Medical College of Cornell University at The Burke Medical Research Institute, White Plains, NY 10605, USA. bconti@burke.org
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pubmed:publicationType |
Journal Article
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