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The effects of colony-stimulating factor-1 on the distribution of mononuclear phagocytes in the developing
P Roth1, M G Dominguez, E R Stanley
1Division of Neonatology, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA.
Abstract:
Colony-stimulating factor-1 (CSF-1), the primary regulator of mononuclear phagocyte (Mphi) 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 Mphi 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 Mphi identified and quantified. In the presence of circulating maternal CSF-1 (+/csfmop mother), Mphi 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), Mphi 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 Mphi 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 Mphi developed in the complete absence of CSF-1, other factors must also be involved in the regulation of macrophage development.
Insights
Maternal colony-stimulating factor-1 (CSF-1) crosses the placenta, aiding fetal mononuclear phagocyte (Mphi) development. Its absence impacts Mphi development differently across fetal tissues, suggesting other regulatory factors are involved.
Area of Science:
- Immunology
- Developmental Biology
- Hematopoiesis
Background:
- Colony-stimulating factor-1 (CSF-1) regulates mononuclear phagocyte (Mphi) production.
- CSF-1 exists as a soluble or membrane-bound molecule.
- Understanding CSF-1's role in perinatal development is crucial.
Purpose of the Study:
- To determine if maternal CSF-1 transfers across the placenta.
- To investigate the role of CSF-1 in perinatal Mphi development.
- To identify tissue-specific effects of CSF-1 deficiency on Mphi populations.
Main Methods:
- Injected pregnant mice with radiolabeled CSF-1 to track placental transfer.
- Utilized CSF-1-deficient osteopetrotic (csfmop/csfmop) mice to study Mphi development.
- Genotyped offspring and quantified Mphi in various fetal tissues.
Main Results:
- Biologically active CSF-1 successfully crossed the placenta, with peak concentrations in fetal tissues within 10 minutes.
- In the presence of maternal CSF-1, Mphi development in csfmop/csfmop livers was nearly complete at birth.
- Mphi development was significantly reduced in spleen, kidney, and lung of csfmop/csfmop offspring from CSF-1 deficient mothers, but liver Mphi were less affected.
Conclusions:
- CSF-1 is essential for perinatal Mphi development in most fetal tissues.
- Maternal CSF-1 can compensate for the absence of local CSF-1 production in a tissue-specific manner, particularly in the liver.
- The development of some Mphi in the complete absence of CSF-1 indicates the involvement of additional regulatory factors.
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