Long-term overexpression of human granulocyte colony-stimulating factor in transgenic mice: persistent neutrophilia with no increased mortality for more than one year

Cytokine. 2000 Jun;12(6):630-5. doi: 10.1006/cyto.2000.0669.

Abstract

To investigate possible adverse consequences of persistent neutrophil overproduction, mice transgenic for human granulocyte colony-stimulating factor (hG-CSF) were studied for more than 1 year. They showed marked granulocytopoiesis and neutrophilia. Continuous medullary and extramedullary granulocytopoiesis resulted in marked changes in bone and liver. In the liver, haemorrhage and focal necrosis and a few haemangiosarcomas were present, presumably caused by the destructive granulocytopoiesis. Despite the high incidence of lung infiltration by mature neutrophils, lung lesions rarely appeared. Although there was a persistent increase in neutrophils, mortality of the mice did not differ from that of non-transgenic littermates at least within 1 year after birth. Factors other than overproduction of G-CSF and extensive neutrophilia could be required for the development of neutrophil-mediated acute and chronic tissue damage.

MeSH terms

  • Animals
  • Death
  • Female
  • Granulocyte Colony-Stimulating Factor / genetics*
  • Granulocyte Colony-Stimulating Factor / physiology
  • Humans
  • Leukocyte Count
  • Lymphocyte Count
  • Male
  • Mice
  • Mice, Transgenic
  • Neutrophil Infiltration / physiology*
  • Neutrophils / pathology*
  • Neutrophils / physiology*
  • Organ Specificity

Substances

  • Granulocyte Colony-Stimulating Factor