Synergistic inhibition of human marrow granulocyte-macrophage progenitor cells by prostaglandin E and recombinant interferon-alpha, -beta, and -gamma and an effect mediated by tumor necrosis factor

J Immunol. 1988 Jan 15;140(2):479-84.

Abstract

The effects of prostaglandin E (PGE) and recombinant human interferon-alpha, -beta, and -gamma alone and in combination were tested for their effects on the proliferation of human bone marrow granulocyte-macrophage colony-forming units (GM-CFU). When tested alone, both classes of cytokines inhibited GM-CFU proliferation. In combination, PGE and all three types of recombinant interferons synergized in their ability to inhibit GM-CFU proliferation. Progressive enrichment for marrow GM-CFU indicated that the synergistic effects of PGE and interferon were dependent upon the presence of marrow-adherent cells. Studies using conditioned media from marrow-adherent cells prepared in the presence of interferon-alpha, -beta, and -gamma indicated that adherent cells produced a soluble factor in the presence of interferons that subsequently synergized with PGE in inhibiting GM-CFU proliferation. Neutralization of this conditioned media with a monoclonal antibody to tumor necrosis factor abrogated the synergistic inhibition of GM-CFU observed in the presence of PGE. The addition of recombinant tumor necrosis factor and PGE to accessory cell-depleted bone marrow resulted in synergystic inhibition of GM-CFU proliferation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Antibodies, Monoclonal / physiology
  • Antigen-Presenting Cells / physiology
  • Bone Marrow / physiology
  • Bone Marrow Cells*
  • Cell Adhesion
  • Dinoprostone
  • Drug Synergism
  • Granulocytes / drug effects
  • Granulocytes / physiology
  • Hematopoietic Stem Cells / drug effects*
  • Hematopoietic Stem Cells / physiology
  • Humans
  • Interferon Type I / pharmacology*
  • Interferon-gamma / pharmacology*
  • Macrophages / drug effects
  • Macrophages / physiology
  • Prostaglandins E / pharmacology*
  • Recombinant Proteins / pharmacology
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Antibodies, Monoclonal
  • Interferon Type I
  • Prostaglandins E
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Dinoprostone