Granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor: differential action on incisional wound healing.

Abstract

Granulocyte-macrophage colony-stimulating factor (GM-CSF) specifically stimulates granulocyte, macrophage, and eosinophil colonies; granulocyte colony-stimulating factor (G-CSF) acts directly on neutrophil-restricted progenitor cells in their proliferation. Those cells have been implicated in the process of wound healing. Paired 6 cm incisions were made on rats; GM-CSF or G-CSF was given systemically (100 micrograms/kg/dose) or locally (30 micrograms/wound). The controls received vehicle alone. Impaired healing was induced by injection of methylprednisolone (30 mg/kg). White blood cells (WBC) were counted at day 2 after treatment. Tissue strips were evaluated for tensiometry and histologic features at days 7 and 14 after wounding. For local GM-CSF treated incisions, the breaking strength was 25% stronger than controls at day 7 (p = 0.004), 36% at day 14 (p < 0.0001), and 42% at day 7 (p = 0.012) in impaired animals. Local G-CSF and systemic GM-CSF and G-CSF increased circulating WBC (p < 0.05), but they had no effects on healing. Histologic studies revealed an increase of wound cellulity at day 7 and day 14 in topical GM-CSF treated wounds. These results suggest GM-CSF is an activator of tissue macrophages and that increasing circulating WBC did not affect wound healing.