Transfer of recombinant human granulocyte colony stimulating factor (rhG-CSF) from the maternal to the fetal circulation is not dependent upon a functional G-CSF-receptor.

Administration of granulocyte colony stimulating factor (G-CSF), a haematopoietic growth factor, to pregnant rats increases neutrophil production in the pups. The mechanism for the placental transfer is unknown, but it has been speculated to involve the placental G-CSF receptor (G-CSFR). The purpose of this study was to test that hypothesis. Pregnant mice were treated with a single subcutaneous dose of 50 microg/kg recombinant human G-CSF (rhG-CSF). Mice with an intact G-CSFR ("wild type", WT) and those with a homozygous deletion in the G-CSFR gene (G-CSFR deficient, "knock-out", KO) were studied. At intervals after injection, fetuses were delivered and maternal blood, amniotic fluid (AF) and fetal blood collected. G-CSF concentrations were measured using an enzyme linked immunosorbent assay specific for human G-CSF. Thirty minutes after injection, G-CSF was measurable in the AF (167+/-50 versus 445+/-217 pg/ml, mean+/-sem, WT versus KO) and fetal plasma (774+/-673 versus 427+/-121 pg/ml, WT versus KO). Peak concentrations occurred 2 h after injection in WT dams (572 542+/-41 262 pg/ml) and 4 h in KO dams (616 100+/-96 300 pg/ml). Therefore, in mice, a functional G-CSFR is not essential for the transfer of rhG-CSF from pregnant dams to their fetuses.