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Rheumatology 2001; 40: 267-273
© 2001 British Society for Rheumatology

Glucocorticoid-mediated repression of inflammatory cytokine production in fibroblast-like rheumatoid synoviocytes is independent of nuclear factor-{kappa}B activation induced by tumour necrosis factor {alpha}

C. W. Han, J. H. Choi1, J. M. Kim, W. Y. Kim, K. Y. Lee1 and G. T. Oh1

Department of Orthopaedic Surgery, College of Medicine, The Catholic University of Korea, Seoul and
1 Genetic Resources Center, Korea Research Institute of Bioscience and Biotechnology, Yusong, Taejon, Korea

Objective. To determine whether steroids inhibit the production of inflammatory cytokines by the inhibition of nuclear factor {kappa}B (NF-{kappa}B) activation in fibroblast-like rheumatoid synoviocytes (FLSs) under inflammatory conditions, and to determine whether steroids stimulate the induction of synthesis of the inhibitory protein I{kappa}B-{alpha} in the anti-inflammatory immune response of these cells.

Methods. Expression of the interleukin-6 (IL-6) and interleukin-1ß (IL-1ß) genes was measured by semi-quantitative reverse transcription–polymerase chain reaction (RT-PCR), and the secreted IL-6 was measured with the enzyme-linked immunosorbent assay. Inhibition of the NF-{kappa}B activation was examined with the electrophoretic mobility shift assay (EMSA). In order to study dexamethasone (DEX)-dependent regulation of I{kappa}B-{alpha} expression, we performed Western blotting before and after stimulation with tumour necrosis factor {alpha} (TNF-{alpha}).

Results. The inflammatory cytokine study showed that DEX suppressed gene expression and the production of protein in FLSs. EMSA demonstrated that identical amounts of NF-{kappa}B were present in the nucleus of the FLSs stimulated by TNF-{alpha}, with or without pretreatment with DEX. Treatment of FLSs with DEX did not induce an increase in I{kappa}B-{alpha} sufficient to prevent nuclear translocation of NF-{kappa}B on stimulation with TNF-{alpha}.

Conclusion. DEX may suppress the production of inflammatory cytokines, such as IL-6 and IL-1ß, but it neither prevents the translocation of NF-{kappa}B to the nucleus nor induces the synthesis of I{kappa}B-{alpha} protein in FLSs stimulated by TNF-{alpha}.

KEY WORDS: Dexamethasone, Rheumatoid arthritis, Synoviocytes, NF-{kappa}B, I{kappa}B-{alpha}, TNF-{alpha}, IL-6, IL-1ß.

Correspondence to: G. T. Oh, Genetic Resources Center, Korea Research Institute of Bioscience and Biotechnology, P. O. Box 115, Yusong, Taejon 305–600, Korea


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