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Production of granulocyte colony-stimulating factor in vitro by monocytes
from preterm and term neonates [see comments]
KR Schibler, KW Liechty, WL White and RD Christensen
Division of Human Development and Aging and Neonatology, University of Utah
School of Medicine, Salt Lake City.
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-1 alpha (IL-1 alpha) or
lipopolysaccharide (LPS), quantified G-CSF concentrations in cell
supernatants and G-CSF mRNA in cell lysates. When stimulated with plateau
concentrations of IL-1 alpha for 24 hours, G-CSF concentrations were higher
in supernatants of adult cells (8,699 +/- 5,529 pg/10(6) monocytes) than in
those from term infants (2,557 +/- 442 pg, P < .05) or from preterm
infants (879 +/- 348 pg, P < .05 v adults). When stimulated with plateau
concentrations of LPS, supernatants of monocytes from preterm neonates had
less G-CSF than did those from term neonates or adults. G-CSF mRNA content
was low in cells from preterm infants, higher in those from term infants,
and highest in those from adults. On the basis of the in vitro studies, we
speculated that serum G-CSF concentrations might be less elevated in
neutropenic neonates than in neutropenic adults. Indeed, serum
concentrations were relatively low in all nonneutropenic subjects; 92 +/-
34 pg/mL (mean +/- SEM) in 10 preterm neonates, 114 +/- 21 pg/mL in 16 term
neonates, and 45 +/- 13 pg/mL in 11 healthy adults. Serum concentrations
were not elevated in 7 neutropenic neonates (39 +/- 17 pg/mL) but were in 8
neutropenic adults (2101 +/- 942 pg/mL, 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.
Volume 82,
Issue 8,
pp. 2478-2484,
10/15/1993
Copyright © 1993 by The American Society of Hematology
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