| pubmed-article:10681439 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10681439 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:10681439 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:10681439 | lifeskim:mentions | umls-concept:C0765701 | lld:lifeskim |
| pubmed-article:10681439 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
| pubmed-article:10681439 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:10681439 | lifeskim:mentions | umls-concept:C1514503 | lld:lifeskim |
| pubmed-article:10681439 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:10681439 | pubmed:dateCreated | 2000-4-11 | lld:pubmed |
| pubmed-article:10681439 | pubmed:abstractText | IL-18 shares with IL-1 the same family of receptors and several identical signal transduction pathways. Because of these similarities, IL-18 was investigated for its ability to induce prostaglandin E(2) (PGE(2)) synthesis in human peripheral blood mononuclear cells (PBMC), a prominent, proinflammatory property of IL-1. IL-18 was highly active in PBMC by inducing the synthesis of the chemokine IL-8; however, no induction of PGE(2) synthesis nor cyclooxygenase type-2 gene expression was observed in PBMC stimulated with IL-18. In the same cultures, IL-1beta induced a 12-fold increase in PGE(2). Although IL-1beta-induced IL-8 synthesis was augmented 3-fold by IL-18, IL-18 suppressed IL-1beta-induced PGE(2) production by 40%. The suppressive effect of IL-18 on PGE(2) production was mediated by interferon (IFN)-gamma because anti-human IFN-gamma-antibody prevented IL-18-induced reduction in PGE(2). Consistent with these observations, IL-12, a known inducer of IFN-gamma, augmented IL-1beta-induced IFN-gamma but suppressed IL-1beta-induced PGE(2) by 75%. IL-18 binding protein (IL-18BP) is a naturally occurring and specific inhibitor of IL-18. When recombinant IL-18BP was added to PBMC cultures, unexpectedly, spontaneous PGE(2) production increased. PGE(2) production was also increased by the addition of IL-18BP to PBMC stimulated with either IL-1beta or IL-12 and also in whole blood cultures stimulated with Staphylococcus epidermidis. These studies demonstrate that IL-18BP decreases endogenous IL-18 activity by reducing IFN-gamma-mediated responses. | lld:pubmed |
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| pubmed-article:10681439 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10681439 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10681439 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10681439 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:10681439 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:DinarelloC... | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:RubinsteinMM | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:MOER ERE | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:NovickDD | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:WestcottJ YJY | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:ReznikovL LLL | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:FantuzziGG | lld:pubmed |
| pubmed-article:10681439 | pubmed:author | pubmed-author:FrishmanJJ | lld:pubmed |
| pubmed-article:10681439 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10681439 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:10681439 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10681439 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10681439 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10681439 | pubmed:pagination | 2174-9 | lld:pubmed |
| pubmed-article:10681439 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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