Distribution of cells bearing receptors for a colony-stimulating factor (CSF-1) in murine tissues. J Cell Biol 91: 848-853

The Journal of Cell Biology (Impact Factor: 9.83). 01/1982; 91(3 Pt 1):848-53.
Source: PubMed


CSF-1 is a subclass of the colony-stimulating factors that specifically stimulates the growth of mononuclear phagocytes. We used the binding of 125I-CSF-1 at 0 degrees C by single cell suspensions from various murine tissues, in conjunction with radioautography, to determine the frequency of binding cells, their identity, and the number of binding sites per binding cell. For all tissues examined, saturation of binding sites was achieved within 2 h at 2--3 x 10(-10) M 125I-CSF-1. The binding was irreversible and almost completely blocked by a 2 h preincubation with 5 x 10(-10) M CSF-1. 125I-CSF-1 binding was exhibited by 4.3% of bone marrow cells, 7.5% of blood mononuclear cells, 2.4% of spleen cells, 20.5% of peritoneal cells, 11.8% of pulmonary alveolar cells and 0.4% of lymph node cells. Four morphologically distinguishable cell types bound 125I-CSF-1: blast cells; mononuclear cells with a ratio of nuclear to cytoplasmic area (N/C) greater than 1; cells with indented nuclei; and mononuclear cells with N/C less than or equal to 1. No CSF-1 binding cells were detected among blood granulocytes or thymus cells. Bone marrow promyelocytes, myelocytes, neutrophilic granulocytes, eosinophilic granulocytes, nucleated erythroid cells, enucleated erythrocytes, and megakaryocytes also failed to bind. The frequency distribution of grain counts per cell for blood mononuclear cells was homogenous. In contrast, those for bone marrow, spleen, alveolar, and peritoneal cells were heterogeneous. The monocytes in blood or bone marrow (small cells, with either indented nuclei or with N/C greater than 1) were relatively uniformly labeled, possessing approximately 3,000 binding sites per cell. Larger binding cells (e.g., alveolar cells) may possess higher numbers of receptors. It is concluded that CSF-1 binding is restricted to mononuclear phagocytic cells and their precursors and that it can be used to identify both mature and immature cells of this series.

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    • "Colony stimulating factor-1 (CSF-1) is the primary regulator of macrophage differentiation, survival and proliferation in the mouse (Stanley et al., 1978; Cecchini et al., 1994). The CSF-1 receptor (CSF-1R), encoded by the c-fms proto-oncogene (Sherr et al., 1985), is an excellent marker of cells of the monocytic lineage (monoblast → promonocyte → monocyte → macrophage) (Byrne et al., 1981). While it is expressed at low levels on hematopoietic stem cells (Akashi et al., 2003; Sarrazin et al., 2009), its expression increases ∼10 fold at the earliest stage of commitment to the monocytic lineage (colony forming unit– macrophage, CFU-M) and is further up-regulated on their adherent progeny (monoblasts → promonocyte → monocyte → macrophage) (Tushinski et al., 1982; Bartelmez et al., 1989). "
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    ABSTRACT: This unit provides protocols for measuring the abundance and growth of macrophage precursors in agar cultures and the proliferation of isolated mature macrophages in vitro, by either direct cell counting or by DNA measurement. Methods for the immunohistochemical identification of macrophages and the determination of their proliferative status in vivo by immunofluorescence are also included. It also describes methods for characterization of macrophage differentiation through the immunofluorescence analysis of cell-surface expression of CSF-1 receptor.
    Full-text · Article · Feb 2011 · Current protocols in immunology / edited by John E. Coligan ... [et al.]
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    • "At 6 and 48 h PI, using flow cytometric analysis, we counted Gr-1+/CD115− cells (neutrophils) and Gr1+/ CD115+ cells (monocytes) (Fig. 3A). Gr-1 is present on neutrophils and monocytes (Geissmann et al., 2003; Daley et al., 2008), and CD115 (M-CSF receptor, CSF1R) is present only on monocytes and macrophages (Byrne et al., 1981; Sunderkotter et al., 2004; Tacke et al., 2006). We found that at 6 and 48 h PI there were significantly (6 h: P = 0.0172, 48 h: P = 0.0317) fewer circulating neutrophils (Gr-1+/CD115−) in mice receiving G-CSF neutralizing antibodies as compared with mice receiving control IgG (Fig. 3B). "
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    ABSTRACT: Uropathogenic Escherichia coli (UPEC), the causative agent of approximately 85% of urinary tract infections (UTI), is a major health concern primarily affecting women. During infection, neutrophils infiltrate the bladder, but the mechanism of recruitment is not well understood. Here, we investigated the role of UPEC-induced cytokine production in neutrophil recruitment and UTI progression. We first examined the kinetics of cytokine expression during UPEC infection of the bladder, and their contribution to neutrophil recruitment. We found that UPEC infection induces expression of several pro-inflammatory cytokines including granulocyte colony-stimulating factor (G-CSF, CSF-3), not previously known to be involved in the host response to UTI. G-CSF induces neutrophil emigration from the bone marrow; these cells are thought to be critical for bacterial clearance during infection. Upon neutralization of G-CSF during UPEC infection, we found fewer circulating neutrophils, decreased neutrophil infiltration into the bladder and, paradoxically, a decreased bacterial burden in the bladder. However, depletion of G-CSF resulted in a corresponding increase in macrophage-activating cytokines, such as monocyte chemotactic protein-1 (MCP-1, CCL-2) and Il-1beta, which may be key in host response to UPEC infection, potentially resolving the paradoxical decreased bacterial burden. Thus, G-CSF acts in a previously unrecognized role to modulate the host inflammatory response during UPEC infection.
    Full-text · Article · Sep 2008 · Cellular Microbiology
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    • "Colony-stimulating factors (CSFs) are involved in normal progress of hematopoietic progenitor cells into terminal differentiated state [1]. Macrophage-CSF (M-CSF/CSF-1) interacts with a single class of high-affinity receptors and controls the development of macrophages from myeloid progenitors [2] [3] [4]. The receptor for M-CSF is identical to the c-fms protooncogene product (c-Fms) and is endowed with intrinsic tyrosine kinase activity that is transmitted through M-CSF binding. "
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    ABSTRACT: Signal-transducing adaptor protein-2 (STAP-2) is a recently identified adaptor protein as a c-Fms/M-CSF receptor-interacting protein and constitutively expressed in macrophages. Our previous studies also revealed that STAP-2 binds to MyD88 and IKK-alpha/beta, and modulates NF-kappaB signaling in macrophages. In the present study, we examined physiological roles of the interaction between STAP-2 and c-Fms in Raw 264.7 macrophage cells. Our immunoprecipitation has revealed that c-Fms directly interacts with the PH domain of STAP-2 independently on M-CSF-stimulation. Ectopic expression of STAP-2 markedly suppressed M-CSF-induced tyrosine phosphorylation of c-Fms as well as activation of Akt and extracellular signal regulated kinase. In addition, Raw 264.7 cells over-expressing STAP-2 showed impaired migration in response to M-CSF and wound-healing process. Taken together, our findings demonstrate that STAP-2 directly binds to c-Fms and interferes with the PI3K signaling, which leads to macrophage motility, in Raw 264.7 cells.
    Full-text · Article · Aug 2007 · Biochemical and Biophysical Research Communications
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