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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-2-11
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pubmed:abstractText |
Injury to cartilage is a recognized sequela of neutrophil activation in arthritic joints. This study examined the possibility that chondrocytes may play a direct role in intraarticular neutrophil activation. We demonstrate that IL-1 beta-stimulated primary and subcultured human articular chondrocytes, express the gene for the potent neutrophil chemotactic and activating cytokine, IL-8. Expression of IL-8 mRNA is also inducible by TNF-alpha and LPS and, to a lesser degree, by the chondrocyte growth factor, transforming growth factor-beta, but not by platelet-derived growth factor, acidic and basic fibroblast growth factor, or epidermal growth factor. Analysis of IL-1 beta-stimulated cartilage organ cultures by in situ hybridization demonstrates that chondrocytes in all zones of cartilage are rapidly induced to express the IL-8 gene in high copy number. Metabolically labeled IL-1 beta-stimulated chondrocytes synthesize IL-8 de novo, which comigrates on SDS-PAGE with IL-8 produced by synovial fibroblasts. Furthermore, the conditioned media of IL-1 beta-stimulated chondrocytes and cartilage organ cultures contain neutrophil chemotactic activity which is completely neutralized by a specific antibody to IL-8, establishing that a bioactive form of IL-8 is the major secreted neutrophil chemotactic factor. By using a specific RIA, we demonstrate that not only IL-1 beta, but also TNF-alpha and LPS can induce abundant IL-8 secretion from chondrocytes. In conclusion, articular chondrocytes are readily inducible to express the IL-8 gene and secrete biologically active IL-8 which can promote neutrophil-mediated inflammation and cartilage destruction.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
148
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
466-73
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1729366-Arthritis,
pubmed-meshheading:1729366-Base Sequence,
pubmed-meshheading:1729366-Cartilage, Articular,
pubmed-meshheading:1729366-Gene Expression Regulation,
pubmed-meshheading:1729366-Humans,
pubmed-meshheading:1729366-Interleukin-1,
pubmed-meshheading:1729366-Interleukin-8,
pubmed-meshheading:1729366-Lipopolysaccharides,
pubmed-meshheading:1729366-Molecular Sequence Data,
pubmed-meshheading:1729366-Neutrophils,
pubmed-meshheading:1729366-Organ Culture Techniques,
pubmed-meshheading:1729366-RNA, Messenger,
pubmed-meshheading:1729366-Transforming Growth Factor beta,
pubmed-meshheading:1729366-Tumor Necrosis Factor-alpha
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pubmed:year |
1992
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pubmed:articleTitle |
Cartilage and joint inflammation. Regulation of IL-8 expression by human articular chondrocytes.
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pubmed:affiliation |
Sam and Rose Stein Institute for Research on Aging, Department of Medicine, University of California, San Diego, La Jolla 92093.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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