TY - JOUR
T1 - The effects of colony-stimulating factor-1 on the distribution of mononuclear phagocytes in the developing osteopetrotic mouse
AU - Roth, Philip
AU - Dominguez, Melissa G.
AU - Stanley, E. Richard
PY - 1998/5/15
Y1 - 1998/5/15
N2 - Colony-stimulating factor-1 (CSF-1), the primary regulator of mononuclear phagocyte (MΦ) 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, end the 125I-cpm or human CSF-1 concentrations were measured in fetal tissue, placenta, end fetal/maternal sere. Biologically active CSF-1 crossed the placenta end peaked in fetal tissue, placenta, and serum 10 minutes after injection. The role of CSF-1 in perinatal MΦ development was examined by studying the CSF- 1-deficient osteopatrotic (csfm(op)/csfm(op)) mouse. Fetal/neonatal mice, derived from matings of either +/csfm(op) females with csfm(op)/csfm(op) males or the reciprocal pairings, were genotyped end tissue MΦ identified end quantified. In the presence of circulating maternal CSF-1 (+/csfm(op) mother), MΦ development in csfm(op)/csfm(op) liver was essentially complete at birth relative to +/csfm(op) littermates, but significantly reduced in spleen, kidney, and lung. In the absence of circulating maternal CSF-1 (csfm(op)/csfm(op) mother), MΦ numbers at birth were reduced in csfm(op)/csfm(op) liver relative to the offspring of +/csfm(op) mothers, but were similar in spleen, kidney, and lung. We conclude that CSF-1 is required for the perinatal development of most MΦ in these tissues. Compensation for total absence of local CSF-1 production by circulating, maternal CSF-1 is tissue-specific end most prominent in liver, the first fetal organ perfused by placental blood. However, because some MΦ developed in the complete absence of CSF-1, other factors must also be involved in the regulation of macrophage development.
AB - Colony-stimulating factor-1 (CSF-1), the primary regulator of mononuclear phagocyte (MΦ) 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, end the 125I-cpm or human CSF-1 concentrations were measured in fetal tissue, placenta, end fetal/maternal sere. Biologically active CSF-1 crossed the placenta end peaked in fetal tissue, placenta, and serum 10 minutes after injection. The role of CSF-1 in perinatal MΦ development was examined by studying the CSF- 1-deficient osteopatrotic (csfm(op)/csfm(op)) mouse. Fetal/neonatal mice, derived from matings of either +/csfm(op) females with csfm(op)/csfm(op) males or the reciprocal pairings, were genotyped end tissue MΦ identified end quantified. In the presence of circulating maternal CSF-1 (+/csfm(op) mother), MΦ development in csfm(op)/csfm(op) liver was essentially complete at birth relative to +/csfm(op) littermates, but significantly reduced in spleen, kidney, and lung. In the absence of circulating maternal CSF-1 (csfm(op)/csfm(op) mother), MΦ numbers at birth were reduced in csfm(op)/csfm(op) liver relative to the offspring of +/csfm(op) mothers, but were similar in spleen, kidney, and lung. We conclude that CSF-1 is required for the perinatal development of most MΦ in these tissues. Compensation for total absence of local CSF-1 production by circulating, maternal CSF-1 is tissue-specific end most prominent in liver, the first fetal organ perfused by placental blood. However, because some MΦ developed in the complete absence of CSF-1, other factors must also be involved in the regulation of macrophage development.
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U2 - 10.1182/blood.v91.10.3773
DO - 10.1182/blood.v91.10.3773
M3 - Article
C2 - 9573014
AN - SCOPUS:0032525181
SN - 0006-4971
VL - 91
SP - 3773
EP - 3783
JO - Blood
JF - Blood
IS - 10
ER -