Differential effects of granulocyte‐ and granulocyte‐macrophage colony‐stimulating factors (G‐ and GM‐CSF) on neutrophil adhesion in vitro and in vivo

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Abstract
A direct comparison of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) and granulocyte colony‐stimulating factor (G‐CSF) effects on neutrophil adhesiveness has been carried out. In vitro, GM‐CSF and G‐CSF upregulate neutrophil CD11b to a similar degree (to 227 ± 69%, and 232 ± 70% of control cells, respectively, p< 0.0005), but GM‐CSF is more effective in downregulating neutrophil leucocyte adhesion molecule‐1 (LAM‐1), reducing levels to 33 ± 4% (p< 0.0005), while G‐CSF causes a fall to only 65 ± 17% (pIn vivo, both GM‐CSF and G‐CSF upregulate neutrophil CD11b (to 296 ± 45% and 370 ± 150%, respectively of baseline), but surface levels of LAM‐1 on circulating cells are unchanged. GM‐CSF increased neutrophil adhesion to cultured human endothelium in vitro (from 9.3 ± 0.7% to 15.4 ± 1.3%, pIn vivo, both GM‐CSF and G‐CSF produce a transient leucopenia, but recovery of peripheral counts occurs much earlier (by 60 minutes) with G‐CSF, than with GM‐CSF (only 50% of cells have demarginated at 120 min). GM‐CSF appears to be greater proadhesive agonist for neutrophils than G‐CSF.

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