Cytokine regulation of neuronal survival

J Neurochem. 1992 Feb;58(2):454-60. doi: 10.1111/j.1471-4159.1992.tb09743.x.


Interleukin-1 is a cytokine involved in the immune response to infection and inflammation as well as a growth promotor for several cell types. Interleukin-1-like immunoreactive material has been found in the nervous system. We now show that antisera, which blocked the T-cell proliferative effects of interleukin-1 alpha, decreased neuronal cell counts (to 40% of control) in dissociated spinal cord cultures derived from fetal mice. This neuronal loss was prevented by addition of interleukin-1 alpha, and to a lesser extent by interleukin-1 beta. Exogenous interleukin-1 alpha increased the survival of neurons when added to cultures in which the electrical activity was blocked with tetrodotoxin, whereas no such cytokine-related increase in neuronal survival was observed in electrically active cultures. The antiserum-induced death could also be prevented by cotreatment of the cultures with 0.1 nM vasoactive intestinal peptide, a substance that induces the secretion of neuronal trophic factors from nonneuronal spinal cord cells and thereby increases neuronal survival in electrically inactive cultures. These studies indicate that the cytokine interleukin-1, or an immunologically cross-reactive protein, can increase neuronal survival.

MeSH terms

  • Animals
  • Cell Division
  • Cell Survival / drug effects
  • Cytokines / physiology*
  • Immune Sera / immunology
  • Immune Sera / physiology
  • Interleukin-1 / immunology
  • Interleukin-1 / pharmacology
  • Neurons / physiology*
  • T-Lymphocytes / cytology
  • Vasoactive Intestinal Peptide / pharmacology


  • Cytokines
  • Immune Sera
  • Interleukin-1
  • Vasoactive Intestinal Peptide