Contribution of tumour necrosis factor α and interleukin (IL) 1β to IL6 production, NF-κB nuclear translocation, and class I MHC expression in muscle cells: in vitro regulation with specific cytokine inhibitors. Issue 9 (24th February 2005)

• Record Type: Journal Article
• Authors: Chevrel, G; Granet, C; Miossec, P
• Is Part Of: Annals of the rheumatic diseases. Volume 64:Issue 9(2005)
• Page Start: 1257
• Page End: 1262
• Publication Date: 2005-02-24
• Subjects: DMEM, Dulbecco's modified Eagle's medium -- ELISA, enzyme linked immunosorbent assay -- FACS, fluorescence activated cell sorter -- FCS, fetal calf serum -- FITC, fluorescein isothiocyanate -- IL1β, interleukin 1β -- IIM, idiopathic inflammatory myopathies -- MHC, major histocompatibility complex -- NF-κB, nuclear factor κB -- PBS, phosphate buffered saline -- RA, rheumatoid arthritis -- sR, soluble receptor(s) -- TNFα, tumour necrosis factor α; interleukin 1 -- myoblasts -- myositis -- soluble receptors -- tumour necrosis factor α; Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/ard.2004.032359
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Objective: To evaluate the effect of tumour necrosis factor α (TNFα), interleukin (IL) 1β, and their respective inhibitors the p75 TNFα soluble receptor (sTNFR) and the type II sIL1βR (sIL1RII) on whole muscle and isolated myoblast activation. Methods: Normal muscle samples were stimulated for 7 days with TNFα alone or in combination with IL1β, and myoblasts from these samples for 48 hours. IL6 production was measured by ELISA. Nuclear translocation of NF-κB was analysed by immunofluorescent staining and class I MHC expression by FACS. Results: TNFα and IL1β induced IL6 production by normal muscle samples and myoblasts, the action of TNFα being more potent on muscle samples. Their soluble receptors (1 μg/ml) decreased this production. Suboptimal concentrations of TNFα and IL1β induced NF-κB translocation. sTNFR markedly down regulated TNFα-induced translocation while sIL1RII was less potent on IL1β-induced activation. NF-κB translocation induced by the combination of optimal concentrations of TNFα and IL1β was completely inhibited by their soluble receptors. TNFα and to a lesser extent IL1β induced class I MHC expression by myoblasts and this effect was completely inhibited by their respective soluble receptors. Conclusion: These results suggest that TNFα and IL1β should be targeted for myositis treatment.