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Interaction between interleukin-1 and ciliary neurotrophic factor in the regulation of neuroblastoma cell functions |
European Cytokine Network. Volume 8, Number 4, 367-74, December 1997, Review
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 Résumé
 Summary
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Author(s) : Paola Bossù, Paolo Ruggiero, Giovanni Macchia, Giovanni Maurizi, Cinzia Bizzarri, Detlef Neumann, Aldo Tagliabue, Diana Boraschi, Research Center Dompé SpA. Via Campo di Pile, 1-67100 L’Aquila, Italy, Consorzio Biolaq, Via Campo di Pile, 1-67100 L’Aquila, Italy, Molekularpharmakologie, Medizinische Hochschule, Hannover, Germany.. |
Summary : Human neuroblastoma cells SK-N-SH express significant numbers of IL-1R type I on their surface, as detected by saturation binding and RT-PCR, and are responsive to IL-1? activation by producing inflammatory cytokines IL-6 and IL-8. IL-1β can also have an indirect effect on nervous cell functions, since it is able to modulate the stimulus-induced increase of intracellular Ca++ levels, one of the first steps of the cell activation mechanism. In fact, on SK-N-SH neuroblastoma cells, IL-1β can inhibit the Ca++ increase induced by stimulation of acetylcholine receptors with carbachol. In parallel to IL-1β, the neurotrophic factor CNTF also shows an inhibitory effect on carbachol-stimulated Ca++ increase in CNTFRα-expressing SK-N-SH cells. However, when simultaneously present, the two cytokines cross-inhibit, thus allowing full cell activation in response to the cholinoceptor agonist. The inhibitory effect of CNTF on IL-1? activities on nervous cells was confirmed in the IL-6 production assay. In fact, while CNTF could not induce IL-6 production, it could strongly inhibit cytokine production in response to IL-1β in SK-N-SH cells. The down-modulation of IL-1 effects by CNTF could be one of the mechanisms controlling the extent of the inflammatory reaction at the nervous system level. |
Keywords : interleukin-1, calcium fluxes, CNTF, IL-1 receptors, inflammatory cytokines. |
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