Production of granulocyte colony-stimulating factor in vitro by monocytes from preterm and term neonates

Abstract

We postulated that defective generation of granulocyte colony-stimulating factor (G-CSF) by cells of newborn infants might underlie their deficiencies in upregulating neutrophil production and function during bacterial infection. To test this, we isolated monocytes from the blood of preterm neonates, term neonates, and adults and, after stimulation with various concentrations of interleukin-1α (IL-1α) or lipopolysaccharide (LPS), quantified G-CSF concentrations in cell supernatants and G-CSF mRNA in cell lysates. When stimulated with plateau concentrations of IL-1α for 24 hours, G-CSF concentrations were higher in supernatants of adult cells (8,699 ± 5,529 pg/106 monocytes) than in those from term infants (2,557 ± 442 pg, P < .05) or from preterm infants (879 ± 348 pg, P < .05 v healthy adults). Other studies suggested that the lower G-CSF production in neonates is not counterbalanced by a heightened sensitivity of G-CSF-responsive progenitors to G-CSF. Therefore, we speculate that newborn infants, particularly those delivered prematurely, generate comparatively low quantities of G-CSF after inflammatory stimulation, and that this might constitute part of the explanation for their defective upregulation of neutrophil production and function during infection. © 1993 by The American Society of Hematology.