Effects of colony-stimulating factors (CSFs) on neutrophil apoptosis: possible roles at inflammation site

We found that granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) had different effects on the apoptosis of human mature neutrophils induced by anti-Fas antibody. GM-CSF suppressed this process and neutrophils retained their functions of superoxide production and enzyme release against invasion of microorganisms. In contrast, G-CSF had a weaker effect on the anti-Fas antibody-induced neutrophil apoptosis than GM-CSF, with neutrophil function suppressed in proportion to the apoptosis. GM-CSF produced by satellite cells at the inflammatory site may inhibit apoptosis and the neutrophils may maintain their primed functions to kill the invading microorganisms. G-CSF produced by fibroblasts or endothelial cells may work in another fashion by increasing the number of neutrophils more effectively than GM-CSF. GM-CSF and G-CSF may exert different effects on neutrophils at the inflammatory sites in the human body.