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Effect of stem cell factor with and without granulocyte colony- stimulating
factor on neonatal hematopoiesis: in vivo induction of newborn myelopoiesis
and reduction of mortality during experimental group B streptococcal sepsis
MS Cairo, JM Plunkett, A Nguyen and C van de Ven
Division of Hematology/Oncology, Children's Hospital of Orange County,
Orange, CA 92668.
Neonatal hematopoiesis and host defense are developmentally immature and
under states of increased demand predispose the newborn to peripheral
cytopenias and depletion of bone marrow storage pool reserves. We have
previously demonstrated that recombinant human granulocyte
colony-stimulating factor (rhG-CSF) can significantly modulate neonatal rat
granulopoiesis and act synergistically with antibiotic therapy to reduce
the mortality rate during experimental group B streptococcal sepsis. Stem
cell factor (SCF) has been shown to stimulate early hematopoietic
progenitor cells and, in the presence of lineage-specific CSFs, enhance
committed progenitor cell proliferation. In the present study we examined
the in vivo neonatal hematologic effects of recombinant rat (rr) SCF (14
days), simultaneous rrSCF + rhG- CSF (14 days), and sequential combination
of rrSCF (7 days) + rhG-CSF (7 days). Sprague-Dawley newborn rats (less
than or equal to 24 hours) were injected intraperitoneal (IP) x 14 days
with the above combinations. rrSCF (0 to 200 micrograms/kg/d) had a
negligible effect on the peripheral platelet count and absolute neutrophil
count (ANC) but the diminution in the hematocrit during the first 10 days
of treatment was less pronounced (P = .0001). However, the simultaneous use
of rrSCF + rhG-CSF synergistically increased the circulating day 6 to 13
ANC (P = .001). Similarly, sequential rrSCF + rhG-SCF also had a
synergistic significant effect during the second week of therapy on the
circulating ANC (P = .01). The bone marrow neutrophil storage and
proliferative pools were also significantly increased in newborn rats
treated with rrSCF + rhG-CSF versus rhG-CSF (P = .02). The bone marrow and
liver/spleen CFU-GM pool was unchanged; however, the CFU-GM proliferative
rates were significantly increased in the rrSCF + rhG-CSF group (P = .04).
rrSCF also induced a significant increase in the bone marrow and
liver/spleen mast cell pool (P = .002). Lastly, rrSCF x 14 days +/- rhG-CSF
significantly reduced the mortality rate at 48 and 120 hours after
experimental group B streptococcus sepsis (P = .03 and .05, respectively).
These data suggest that combination SCF + G-CSF therapy compared with G-CSF
alone significantly increases the neonatal rat peripheral neutrophil count,
bone marrow myeloid pools and proliferative rates, and induces a reduction
in the mortality rate during experimental bacterial sepsis. SCF therapy may
have future potential applications in the modulation of human neonatal
hematopoiesis and host defense.
Volume 80,
Issue 1,
pp. 96-101,
07/01/1992
Copyright © 1992 by The American Society of Hematology
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