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.
Hu
B
B
Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Japan.
Yasui
K
K
D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation; D009113:Muramidase / Q000378:metabolism; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D011994:Recombinant Proteins / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism; D019014:fas Receptor / Q000276:immunology
D000911:Antibodies, Monoclonal; D011994:Recombinant Proteins; D019014:fas Receptor; D013481:Superoxides; D016179:Granulocyte Colony-Stimulating Factor; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D009113:Muramidase