Regular article
Effect of IL-13 on cytokines, cytokine receptors and inhibitors on human osteoarthritis synovium and synovial fibroblasts

https://doi.org/10.1053/joca.1997.0091Get rights and content
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Abstract

Objective: In this study we investigated the effect of interleukin-13 (IL-13), an anti-inflammatory cytokine, for potential therapeutic use in osteoarthritis (OA).

Design: We examined the effect of IL-13 on the synthesis and expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-1 receptor antagonist (IL-1Ra) and stromelysin-1 on human OA synovial membrane inex vivocultures. In addition, we explored the effect of IL-13 on both the IL-1 receptor (IL-1R) and TNF-receptor (TNF-R) systems on OA synovial fibroblasts. This included determination of the levels of IL-1β and TNF-α receptor binding, IL-1Ra and TNF-soluble receptors 55 and 75 (TNF-sR55 and TNF-sR75).

Results: In OA synovial membrane treated with LPS, IL-13 inhibited the synthesis of IL-1β, TNF-α and stromelysin-1, but increased IL-1Ra production. In addition, IL-13 reduced the level of IL-1β mRNA and stimulated the level of IL-1Ra mRNA. In synovial fibroblasts, IL-13 decreased the level of IL-1 binding, an effect related to the increased production of IL-1Ra. Although IL-13 had no effect on the TNF-R level, this cytokine markedly decreased the shedding of TNF-R75.

Conclusion: These experiments suggest that IL-13 is potentially useful in the therapeutic treatment of OA, as it could regulate the major pathological process of this disease by reducing the production of proinflammatory cytokines and metalloproteases, and favoring the production of IL-1Ra.

Keywords

IL-13, Osteoarthritis, Synovial membrane, Proinflammatory cytokines

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This study was supported by the Medical Research Council of Canada.

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Please address all correspondence and reprint requests to: Johanne Martel-Pelletier, Ph.D., Professor of Medicine, Osteoarthritis Research Unit, Notre-Dame Hospital, 1560 Sherbrooke St. East, Montreal, Quebec, Canada H2L 4M1. Tel: (514) 281-6000 ext. 7281. Fax: (514) 896-4680.