Tumor necrosis factor changes sensitivity of differentiation of mouse leukemia M1 cells by lipopolysaccharide

Jpn J Cancer Res. 1990 Apr;81(4):396-402. doi: 10.1111/j.1349-7006.1990.tb02581.x.

Abstract

A clone of mouse leukemia M1 cells was induced to differentiate by lipopolysaccharide (LPS) (LPS-sensitive clone) while another clone of the same cells was resistant (LPS-resistant clone). LPS and lipid A preparations from Pseudomonas diminuta and Pseudomonas vesicularis were as active as Escherichia coli LPS in the induction of differentiation of the LPS-sensitive clone. Synthetic lipid A precursor Ia (compound 406), which has no interleukin 1 (IL-1)-inducing activity toward monocytes, had strong differentiation-inducing activity toward the LPS-sensitive clone. The combined treatment of the LPS-sensitive clone with LPS and recombinant tumor necrosis factor (rTNF) did not further increase the degree of differentiation induced by LPS alone. By contrast, the LPS-resistant clone was markedly induced to differentiate by LPS in the presence of rTNF. Combined treatment of the LPS-resistant clone with LPS and other cytokines such as recombinant IL-1 alpha, recombinant granulocyte colony-stimulating factor, and interferon-gamma was not effective in inducing marked synergistic differentiation. These results raise the possibility that rTNF changes the sensitivity of M1 cells to induction of differentiation by LPS.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation / drug effects*
  • Clone Cells / physiology
  • Clone Cells / ultrastructure
  • Drug Resistance
  • Drug Synergism
  • Humans
  • Leukemia, Myeloid / pathology*
  • Leukemia, Myeloid / physiopathology
  • Lipid A / pharmacology
  • Lipopolysaccharides / pharmacology
  • Mice
  • Receptors, Cell Surface / metabolism
  • Receptors, Tumor Necrosis Factor
  • Structure-Activity Relationship
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Lipid A
  • Lipopolysaccharides
  • Receptors, Cell Surface
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha