Inhibition by interleukin-1 of the action of erythropoietin on erythroid precursors and its possible role in the pathogenesis of hypoplastic anaemias

Br J Haematol. 1987 Sep;67(1):11-7. doi: 10.1111/j.1365-2141.1987.tb02289.x.


Highly purified and cloned preparations of interleukin-1 (IL-1) were found to antagonize the capacity of erythropoietin (Epo) to stimulate the proliferation of mouse spleen and bone marrow erythroid precursor cells (EPC) in culture. Cloned murine IL-1 and purified and cloned human IL-1 alpha and IL-1 beta were approximately equipotent in this assay. IL-1 inhibited the proliferation response of EPC even when added as long as 17 h after Epo, suggesting that IL-1 does not affect binding of Epo to receptors or biochemical events following shortly thereafter. Indomethacin did not influence the inhibitory effect of IL-1 on Epo-induced proliferation, and PGE2 had no demonstrable effect on the process. Tumor-necrosis factor-alpha and interferons beta 1, and gamma did not affect Epo-induced proliferation. It is suggested that IL-1 mediated antagonism of the effects of Epo on erythroid precursors is a factor in the pathogenesis of many types of hypoplastic anaemia, including those associated with infections, rheumatoid arthritis and systemic lupus erythematosus, giant-cell arteritis, graft-versus-host disease and disorders associated with lymphocyte-mediated suppression of erythropoiesis.

MeSH terms

  • Anemia / etiology
  • Anemia, Aplastic / pathology*
  • Animals
  • Bone Marrow / pathology*
  • Cell Division / drug effects
  • Cells, Cultured
  • Erythroblasts / drug effects
  • Erythropoietin / antagonists & inhibitors*
  • Female
  • Growth Inhibitors / pharmacology
  • Hematopoietic Stem Cells / drug effects*
  • Interleukin-1 / pharmacology*
  • Mice
  • Spleen / pathology*
  • Tumor Necrosis Factor-alpha / pharmacology


  • Growth Inhibitors
  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Erythropoietin