Control of fecal peritoneal infection in mice by colony-stimulating factors

J Infect Dis. 1996 Oct;174(4):790-9. doi: 10.1093/infdis/174.4.790.

Abstract

Granulocyte colony-stimulating factor (G-CSF) recruits and primes neutrophilic granulocytes. The role of endogenous and exogenous G-CSF was examined in a murine fecal peritoneal infection model characterized by rapid production of high levels of circulating G-CSF. Pretreatment with anti-murine G-CSF for 5 days reduced neutrophil counts by 50% and sensitized mice to sublethal peritonitis. There were more aerobic bacteria in livers of antiserum-pretreated animals but fewer neutrophils in peritoneal cavities. Pretreatment with 100 micrograms/kg recombinant murine G-CSF intravenously for 2 days raised neutrophil counts 5-fold and significantly protected animals against lethal peritonitis. A similar prophylactic administration of murine granulocyte-macrophage (GM)-CSF neither augmented leukocyte numbers nor protected infected mice. These results show a dissociation between the pharmacologic properties of GM-CSF and G-CSF and demonstrate the crucial role of endogenous G-CSF in controlling neutrophil-dependent defense against bacterial invasion in infection.

MeSH terms

  • Animals
  • Bacterial Infections / therapy*
  • Feces / microbiology
  • Female
  • Granulocyte Colony-Stimulating Factor / blood
  • Granulocyte Colony-Stimulating Factor / physiology
  • Granulocyte Colony-Stimulating Factor / therapeutic use*
  • Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use
  • Male
  • Mice
  • Neutrophils / physiology
  • Peritonitis / therapy*
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Tumor Necrosis Factor-alpha
  • Granulocyte Colony-Stimulating Factor
  • Granulocyte-Macrophage Colony-Stimulating Factor