Granulocyte colony-stimulating factor in preterm and term pregnancy, parturition, and intra-amniotic infection

Objective: To determine the sources of granulocyte colony-stimulating factor (G-CSF) in amniotic fluid and to examine its relation to labor and clinically diagnosed intra-amniotic infection. Methods: We assessed G-CSF and G-CSF receptor expression in placentas ( n = 50) from 5–40 weeks’ gestation, and G-CSF concentrations were measured in amniotic fluid ( n = 146), bronchoalveolar lavage fluid ( n = 8), and paired maternal serum, cord blood, neonatal serum, and neonatal urine samples ( n = 16). Results: Immunohistochemical staining and messenger RNA analysis showed placental expression of G-CSF and G-CSF receptor throughout gestation. The number of decidual stromal cells expressing G-CSF receptor was significantly higher in women with intra-amniotic infection compared with women without infection (27 ± 2 versus 18 ± 3 cells per high power field, P = .02). Amniotic fluid concentrations of G-CSF were not significantly different in noninfected preterm compared with term samples (1708 ± 1673 versus 1612 ± 2100 pg/mL, P = .9). Labor was not associated with a significant increase in amniotic fluid G-CSF concentrations (1864 ± 3151 versus 1612 ± 2100 pg/mL, P = .77, term labor versus no labor; 3335 ± 5364 versus 1708 ± 1673 pg/mL, P = .09, preterm). Concentrations of G-CSF in maternal serum, amniotic fluid, bronchoalveolar lavage fluid, and neonatal urine were increased during intra-amniotic infection (all P < .05). Conclusion: Amniotic fluid G-CSF concentrations were similar in preterm and term pregnancies and were not significantly influenced by labor. Intra-amniotic infection was associated with an increased number of placental cells expressing the G-CSF receptor and higher concentrations of G-CSF in amniotic fluid, maternal serum, neonatal urine, and neonatal bronchoalveolar lavage samples.