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The Effects of Colony-Stimulating Factor-1 on the Distribution of
Mononuclear Phagocytes in the Developing Osteopetrotic Mouse
Philip Roth,
Melissa G. Dominguez, and
E. Richard Stanley
From the Division of Neonatology, Department of Pediatrics and
Department of Developmental and Molecular Biology, Albert Einstein
College of Medicine, Bronx, NY.
Colony-stimulating factor-1 (CSF-1), the primary regulator of
mononuclear phagocyte (M ) production, exists as either a circulating or cell surface, membrane-spanning molecule. To establish
transplacental transfer of maternal CSF-1, gestational day-17 mothers
were injected intravenously with 125I-mouse CSF-1 or human
rCSF-1, and the 125I-cpm or human CSF-1 concentrations were
measured in fetal tissue, placenta, and fetal/maternal sera.
Biologically active CSF-1 crossed the placenta and peaked in fetal
tissue, placenta, and serum 10 minutes after injection. The role of
CSF-1 in perinatal M development was examined by studying the
CSF-1-deficient osteopetrotic
(csfmop/csfmop) mouse. Fetal/neonatal
mice, derived from matings of either +/csfmop
females with csfmop/csfmop males or the
reciprocal pairings, were genotyped and tissue M identified and
quantified. In the presence of circulating maternal CSF-1
(+/csfmop mother), M development in
csfmop/csfmop liver was essentially
complete at birth relative to +/csfmop
littermates, but significantly reduced in spleen, kidney, and lung. In
the absence of circulating maternal CSF-1
(csfmop/csfmop mother), M numbers at
birth were reduced in csfmop/csfmop
liver relative to the offspring of +/csfmop
mothers, but were similar in spleen, kidney, and lung. We conclude that
CSF-1 is required for the perinatal development of most M in these
tissues. Compensation for total absence of local CSF-1 production by
circulating, maternal CSF-1 is tissue-specific and most prominent in
liver, the first fetal organ perfused by placental blood. However,
because some M developed in the complete absence of CSF-1, other
factors must also be involved in the regulation of macrophage
development.
Blood, Vol. 91 No. 10 (May 15), 1998:
pp. 3773-3783
© 1998 by The American Society of Hematology.
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