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© 1991 British Society for Rheumatology

research-article

ROLE OF TNF{alpha}, IN RELATION TO IL-1 AND IL-6 IN THE PROTEOGLYCAN TURNOVER OF HUMAN ARTICULAR CARTILAGE

B. WILBRINK, J. J. NIETFELD, W. DEN OTTER*, J. L. A. M. VAN ROY, J. W. J. BIJLSMA and O. HUBER-BRUNING

Department of Rheumatology, University Hospital Utrecht The Netherlands
*Department of Pathology, University Hospital Utrecht The Netherlands

Correspondence to: Correspondence to Dr B. Wilbrink, University Hospital, Department of Rheumatology, F.02. 223, P. O. Box 85500, 3508 GA Utrecht, The Netherlands.

In both young and old human articular cartilage explants, TNF{alpha} induced a concentration-dependent, reversible suppression of the proteoglycan (PG) synthesis. Young cartilage was more sensitive to TNF{alpha} than old cartilage: 50% suppression of PG synthesis was reached at a TNF{alpha} concentration of 5 U/ml for young and 30 U/ml for old cartilage, whereas at 103 U/ml the PG synthesis of young cartilage was blocked and that of old cartilage suppressed by 80%. These inhibition levels of PG synthesis resulted in 25% PG depletion of the explants after 8 days of culture. The release of cartilage PG not enhanced. TNF{alpha} induced no detectable amounts of IL-1 (<0.01 U) in young or old cartilage but did induce IL-6 production. The induced amounts of IL-6 were higher in young than in old cartilage but no dose-dependency was evident. Antibodies to neither IL-1 nor IL-6 had any influence on the TNF{alpha}-induced suppression of PG synthesis. The combination of TNF{alpha} and IL-1 led to an additive inhibition of PG synthesis which had no relationship to induced IL-6. TNF{alpha} was about 100-fold less active than IL-1.

KEY WORDS: Explant culture, Cytokines, Bioassay


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