Phagocytosis and inflammatory stimuli induce GM-CSF mRNA in macrophages through posttranscriptional regulation

Cell. 1987 Feb 27;48(4):671-9. doi: 10.1016/0092-8674(87)90245-5.

Abstract

Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) is a powerful growth and differentiation factor which acts on hematopoietic progenitor cells and also activates differentiated granulocytes and macrophages. This study shows that mouse peritoneal macrophages can be induced to accumulate GM-CSF mRNA and to release GM-CSF by inflammatory agents (lipopolysaccharide, fetal calf serum, thioglycolate broth); phagocytosis; and adherence in the presence of fibronectin. GM-CSF mRNA accumulation, which is totally prevented by the corticosteroid dexamethasone and by interferon-gamma, is not accompanied by changes in the gene's transcriptional level. No interleukin 3 (multi-CSF) mRNA is detectable in induced macrophages. These findings have implications in the understanding of hematopoiesis and of the inflammation and repair process.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation
  • Dexamethasone / pharmacology
  • Fibronectins / pharmacology
  • Hematopoiesis
  • Inflammation / genetics*
  • Inflammation / metabolism
  • Interferon-gamma / pharmacology
  • Interleukin-3 / genetics*
  • Lactoferrin / pharmacology
  • Lipopolysaccharides / pharmacology
  • Macrophages / metabolism*
  • Mice
  • Phagocytosis*
  • Protein Processing, Post-Translational*
  • RNA, Messenger / metabolism*
  • Thioglycolates / pharmacology

Substances

  • Fibronectins
  • Interleukin-3
  • Lipopolysaccharides
  • RNA, Messenger
  • Thioglycolates
  • Dexamethasone
  • Interferon-gamma
  • Lactoferrin