Relationship between TNF-alpha and iron metabolism in differentiating human monocytic THP-1 cells

Br J Haematol. 2000 Sep;110(4):978-84. doi: 10.1046/j.1365-2141.2000.02280.x.

Abstract

The human monocytic cell line THP-1 differentiates along the macrophage line after phorbol-12-myristate-13-acetate (PMA) supplementation and can be stimulated to secrete tumour necrosis factor alpha (TNF-alpha) by interferon gamma (IFN-gamma) addition. We found that, in the early stage of differentiation (1-48 h), PMA induction elicited an upregulation of intracellular H ferritin and H ferritin binding sites and a downregulation of transferrin receptor. In addition, we found that iron administration to PMA-differentiating cells induced the expression of TNF-alpha mRNA and TNF-alpha secretion to levels even higher than those induced by IFN-gamma alone. The iron chelator desferrioxamine showed the opposite effect and reduced TNF-alpha release. In contrast, preincubation of the cells with iron before PMA induction resulted in a decrease of the TNF-alpha secretion induced by IFN-gamma, whereas the opposite was true after preincubation with desferrioxamine. The data support a co-ordinate interaction between iron and TNF-alpha in monocyte macrophages, with an iron-mediated upregulation of TNF-alpha in the early phase of differentiation and an iron-mediated inhibition at later stages. This complex relationship has to be considered in evaluating the effects of iron on inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Binding Sites
  • Blotting, Northern
  • Cell Differentiation
  • Cell Line
  • Chelating Agents / pharmacology
  • Deferoxamine / pharmacology
  • Ferritins / metabolism
  • Humans
  • Inflammation
  • Interferon-gamma / pharmacology
  • Iron / metabolism*
  • Iron / pharmacology
  • Leukemia, Monocytic, Acute / metabolism
  • Leukemia, Monocytic, Acute / pathology
  • Leukemia, Monocytic, Acute / physiopathology
  • Macrophages / cytology
  • Macrophages / drug effects
  • Macrophages / metabolism*
  • Receptors, Transferrin / metabolism
  • Stimulation, Chemical
  • Tetradecanoylphorbol Acetate / pharmacology
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Chelating Agents
  • Receptors, Transferrin
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Ferritins
  • Iron
  • Deferoxamine
  • Tetradecanoylphorbol Acetate