Interaction between interleukin-1 and ciliary neurotrophic factor in the regulation of neuroblastoma cell functions

Eur Cytokine Netw. 1997 Dec;8(4):367-74.


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-1beta activation by producing inflammatory cytokines IL-6 and IL-8. IL-1beta 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-1beta can inhibit the Ca++ increase induced by stimulation of acetylcholine receptors with carbachol. In parallel to IL-1beta, the neurotrophic factor CNTF also shows an inhibitory effect on carbachol-stimulated Ca++ increase in CNTFRalpha-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-1beta 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-1beta 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ciliary Neurotrophic Factor
  • Down-Regulation
  • Humans
  • Inflammation / metabolism*
  • Interleukin-1 / metabolism*
  • Nerve Tissue Proteins / metabolism*
  • Neuroblastoma / metabolism*
  • Neurons / metabolism*
  • Polymerase Chain Reaction / methods
  • Receptors, Interleukin-1 / biosynthesis
  • Transcription, Genetic


  • Ciliary Neurotrophic Factor
  • Interleukin-1
  • Nerve Tissue Proteins
  • Receptors, Interleukin-1