The effects of colony-stimulating factor-1 on the distribution of mononuclear phagocytes in the developing osteopetrotic mouse

Philip Roth, Melissa G. Dominguez, E. Richard Stanley

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3773-3783
Number of pages11
JournalBlood
Volume91
Issue number10
StatePublished - May 15 1998

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Macrophage Colony-Stimulating Factor
Phagocytes
Mothers
Tissue
Liver
Placenta
Fetus
Spleen
Parturition
Kidney
Lung
Macrophages
Blood

ASJC Scopus subject areas

  • Hematology

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The effects of colony-stimulating factor-1 on the distribution of mononuclear phagocytes in the developing osteopetrotic mouse. / Roth, Philip; Dominguez, Melissa G.; Stanley, E. Richard.

In: Blood, Vol. 91, No. 10, 15.05.1998, p. 3773-3783.

Research output: Contribution to journalArticle

Roth, Philip ; Dominguez, Melissa G. ; Stanley, E. Richard. / The effects of colony-stimulating factor-1 on the distribution of mononuclear phagocytes in the developing osteopetrotic mouse. In: Blood. 1998 ; Vol. 91, No. 10. pp. 3773-3783.
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abstract = "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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