IL-18 Is Produced by Articular Chondrocytes and Induces Proinflammatory and Catabolic Responses

IL-18, a cytokine originally identified as IFN-gamma-inducing factor, is a member of the IL-1 family of proteins. Because IL-1alpha and IL-1beta are important mediators in the pathogenesis of arthritis, the present study addresses the expression of IL-18 and its role in regulating in articular chond...

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Bibliographic Details
Published in:The Journal of immunology (1950) 1999-01, Vol.162 (2), p.1096-1100
Main Authors: Olee, Tsaiwei, Hashimoto, Sanshiro, Quach, Jacqueline, Lotz, Martin
Format: Article
Language:English
Subjects:
Arthritis - immunology
Arthritis - metabolism
Arthritis - pathology
Cartilage, Articular - immunology
Cartilage, Articular - metabolism
Cartilage, Articular - pathology
Cell Division - drug effects
Cell Division - immunology
Chondrocytes - drug effects
Chondrocytes - immunology
Chondrocytes - metabolism
Chondrocytes - pathology
Gene Expression Regulation - drug effects
Gene Expression Regulation - immunology
Growth Inhibitors - pharmacology
Growth Inhibitors - physiology
Humans
Interleukin-18 - biosynthesis
Interleukin-18 - genetics
Interleukin-18 - physiology
Knee Joint
Nitric Oxide - biosynthesis
Protein Biosynthesis
Proteoglycans - metabolism
Recombinant Proteins - pharmacology
RNA, Messenger - biosynthesis
Transforming Growth Factor beta - pharmacology
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Summary:IL-18, a cytokine originally identified as IFN-gamma-inducing factor, is a member of the IL-1 family of proteins. Because IL-1alpha and IL-1beta are important mediators in the pathogenesis of arthritis, the present study addresses the expression of IL-18 and its role in regulating in articular chondrocytes. IL-18 mRNA was induced by IL-1beta in chondrocytes. Chondrocytes produced the IL-18 precursor and in response to IL-1 stimulation secreted the mature form of IL-18. Studies on IL-18 effects on chondrocytes showed that it inhibits TGF-beta-induced proliferation and enhances nitric oxide production. IL-18 stimulated the expression of several genes in normal human articular chondrocytes including inducible nitric oxide synthase, inducible cyclooxygenase, IL-6, and stromelysin. Gene expression was associated with the synthesis of the corresponding proteins. Treatment of normal human articular cartilage with IL-18 increased the release of glycosaminoglycans. These finding identify IL-18 as a cytokine that regulates chondrocyte responses and contributes to cartilage degradation.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.162.2.1096