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PubMed1983

Regulation of self-renewal of human T lymphocyte colony-forming units (TL-CFUs).

Formation of human T lymphocyte colonies in semisolid medium from T lymphocyte colony-forming units (TL-CFUs) under stimulation of phytohemagglutinin (PHA) has been reported by several authors. These TL-CFUs were present in unsensitized lymphocyte populations. We report here that such TL-CFUs are capable of renewing themselves. This was observed when colony cells from primary T cell colonies that developed in the presence of PHA were replated in methylcellulose medium containing irradiated autologous leukocytes and PHA. We have also been able to demonstrate serial transfer of TL-CFU for up to six passages. At each passage, colony-forming frequency was determined from the proportional relationship between the number of new colonies obtained and the number of colony cells plated. Examination of the number of new colonies derived from each individual T cell colony ("burst size of TL-CFU") showed that most colonies contained very few new TL-CFU and only a very small number of colonies contained many new TL-CFU. The distribution of burst sizes could be well fitted to a gamma distribution, in agreement with prediction from a stochastic model. We have identified an activity that enhanced the mean TL-CFU burst size three to ten times. This work provides the first evidence in vitro that self-renewal of human T lymphocyte progenitor cells can be stimulated by specific regulatory proteins.

Cell Division↗

PubMed1995

Enhancing and suppressive effects of immunosuppressants cyclosporin A, FK506, and KM2210 on the colony formation of murine bone marrow cells.

Immunosuppressants cyclosporin A (CsA), FK506, and KM2210 modulated colony formations of murine hematopoietic progenitor cells. In a 4-h treatment with CsA, 10 micrograms/ml increased the formation of colony-forming units of mixed lineages (CFU-Mix) but decreased the formation of highly proliferative potential colony-forming units (CFU-HPP); 1 microgram/ml of CsA increased the formations of CFU-HPP, CFU-Mix, and colony-forming units of granulocytes/macrophages (CFU-GM); 0.1 microgram of CsA increased the formation of CFU-Mix and burst-forming units of erythroid lineage (BFU-E). Lower doses of CsA appeared to induce an increase in various colony formations. FK506 increased CFU-HPP and CFU-Mix formations at lower doses. Another immunosuppressant, KM2210, increased CFU-HPP and CFU-GM formations but decreased CFU-Mix and BFU-E formations. In a 24-h treatment, 10 micrograms/ml and 1 microgram/ml of CsA inhibited all the colony formations, but 0.1 microgram/ml of CsA increased CFU-Mix, CFU-GM, and BFU-E formations. Similarly, 100 ng/ml and 10 ng/ml of FK506 decreased all the colony formations but 1 ng/ml of FK506 increased CFU-HPP and CFU-GM formations. KM2210 inhibited all the colony formations. These findings showed that lower doses of CsA and FK506 appeared to increase the colony formations, although higher doses of these drugs decreased the colony formations, similar to the findings in a 4-h treatment. On the other hand, KM2210 showed opposing effects on colony formation with 4-h and 24-h treatments.

Animals↗

PubMed1999

A cost-effective method for the automatic quantitative analysis of fibroblastic colony-forming units.

A great deal of the work characterizing stromal cell precursors in the bone marrow has been performed using the fibroblastic colony-forming unit (CFU-f) assay. However, the assay is limited in its usefulness by the necessity for manual colony counting which means that assay quantitation is highly subjective, time consuming, and much information regarding the colony size is lost. To rectify this, we have developed a computer-automated method for the analysis of CFU-f. Bone marrow cells were cultured at low density and treated with either prostaglandin E(2) (PGE(2)), basic fibroblast growth factor (bFGF), or dexamethasone, and colony formation was assessed by staining with methylene blue. After staining, the dishes were photographed over a light box using a digital camera and the image was then analyzed using Bioimage "Intelligent Quantifier" image analysis software which automatically locates and quantifies each individual colony. The data can then be imported to a spreadsheet program and processed. We have shown that this system can accurately identify, assign coordinates, and quantitate each individual colony. Colony numbers obtained with this method and manually counting showed a linear relationship with a correlation coefficient of 0.99. In addition, using the colony intensity and surface area data, the colony size can be calculated. With this methodology, we have shown that dexamethasone, PGE(2), and bFGF can all modulate total cell numbers in bone marrow stromal cells (BMSC) cultures but modulating both colony number and colony size.

Animals↗

PubMed1998

Changes in macrophage colony-stimulating factor concentration in serum and follicular fluid in in-vitro fertilization and embryo transfer cycles.

OBJECTIVE: To evaluate the changes of macrophage colony-stimulating factor concentration in serum and compare macrophage colony-stimulating factor concentration in follicular fluid (FF) through IVF-ET cycles. DESIGN: Sera and the matched FFs were collected serially through the IVF-ET cycles and analyzed retrospectively with respect to macrophage colony-stimulating factor concentration. SETTING: Department of Obstetrics and Gynecology of Kumamoto University Hospital. PATIENT(S): Ninety-four women underwent 129 cycles of ovulation induction by using GnRH agonist (GnRHa)-hMG-hCG for IVF-ET program. INTERVENTION(S): Serum and FF macrophage colony-stimulating factor concentrations were measured by ELISA. MAIN OUTCOME MEASURE(S): Concentrations of macrophage colony-stimulating factor in serum and FF. RESULT(S): Serum macrophage colony-stimulating factor concentration was gradually increased throughout ovarian stimulation, and reached a peak from the day of oocyte retrieval to 2 days after oocyte retrieval, whereas no significant change in macrophage colony-stimulating factor was observed in cases of poor ovarian response to hMG. The macrophage colony-stimulating factor concentration in follicles was significantly higher than that in sera on the day of oocyte retrieval, and the concentrations in follicles from which oocyte could be retrieved were significantly higher than those from which oocyte could not be retrieved. CONCLUSION(S): These results suggest that gonadotropins lead to an increase in ovarian macrophage colony-stimulating factor production, and that this macrophage colony-stimulating factor production in response to hMG administration is lost in poor ovarian responders. Thus, macrophage colony-stimulating factor may play an important role in the process of follicular maturation and ovulation as an intraovarian regulator.

Adult↗

PubMed1996

Characterisation of colony-stimulating activity in the avian T cell-derived factor, Salmonella enteritidis-immune lymphokine.

This investigation was designed to characterise the specific cytokine activity from the conditioned medium of concanavalin A-stimulated avian T cells derived from Salmonella enteritidis-immune chickens, S enteritidis-immune lymphokine (ILK). Studies were designed to determine first, whether colony-stimulating activity was present in ILK, second, the type(s) of colonies from the bone marrow that were supported in vitro by the potential colony-stimulating factors in ILK and, third, whether colony-stimulating activity was present in serum from chicks treated with ILK and challenged with S enteritidis, and to use physicochemical treatment as a means of identifying the potential colony-stimulating factor(s) in ILK. Both ILK alone and serum from chicks treated with ILK and challenged with S enteritidis caused significant increases in the number of colony-forming units (CFU) from the bone marrow in vitro. After 10 days of incubation, ILK alone supported the in vitro growth of granulocytic bone marrow colonies. The colony-stimulating activity from serum derived from chicks treated with ILK and challenged with S enteritidis peaked two hours after the challenge. When ILK was either heated at 100 degrees C or treated with trypsin or acid and then injected into chicks, all the chicks responded with significant increases in circulating polymorphonuclear leucocytes (PMNs). However, when assayed for in vitro colony-stimulating activity, only trypsinisation destroyed the activity in ILK. The results indicate that a colony-stimulating factor which preferentially supported the growth of granulocytic bone marrow colonies was present in ILK and that the factor was stable to heat and acid but sensitive to trypsin.

Animals↗

PubMed2003

Progenitor cells divide symmetrically to generate new colony-forming cells and clonal heterogeneity.

Self-renewal is the most fundamental property of haemopoietic stem and progenitor cells. However, because of the need to produce differentiated cells, not all cell divisions involve self-renewal. We have used a colony replating assay to follow the fates of individual haemopoietic progenitor cell clones. For this, human myeloid colony-forming cells (CFCs) were cultured by standard methodology. Onset of proliferation and growth rates were established by a video recording method. Individual colonies were replated several times to document the rate of clonal extinction, and the numbers of secondary, tertiary and quaternary CFCs. The clonogenic population exhibited similar kinetics in terms of onset of proliferation and growth rate. Clonal extinction was progressive so that only 30 +/- 7% (mean +/- standard error of the mean; n = 4) of the original primary colonies formed quaternary colonies after the third replating step. However, individual primary CFCs that produced colonies throughout the experiment generated, on average, 40 +/- 8 secondary and tertiary CFCs overall. The values obtained in standard culture conditions were modified when granulocyte colony-stimulating factor (G-CSF) or G-CSF plus interleukin 3 were used to stimulate colony growth, showing that the kinetics of colony formation respond to extrinsic regulation. Examination of the replating potential of individual secondary colonies in the clones demonstrated that they generated different numbers of tertiary colonies. The data best fit a stochastic model of haemopoietic cell development where event probabilities can be modified by extracellular factors.

Cell Division↗

PubMed1981

Quantitative colony method for tumorigenic cells transformed by two distinct strains of Friend leukemia virus.

An in vitro colony method capable of detecting spleen cells malignantly transformed by Friend leukemia virus is described. These colony-forming cells, which form large erythroid colonies (10(4)-10(5) cells) in methylcellulose, can be detected late after infection with either the anemia-inducing (FV-A) or polycythemia-inducing (FV-P) isolates of Friend virus. Colony formation by these cells is dependent only on fetal calf serum as an exogeneous growth factor. The presence of these colony-forming cells in FV-P-infected spleens could not be detected until at least 3 weeks after virus infection, even though the most rapid increase in spleen weight occurred earlier, between 1 and 2 weeks after infection. Thereafter, the numbers of colony-forming cells increased sharply up to 5 weeks after infection with FV-P, beyond which time the mice generally did not survive. After infection with FV-A, colony-forming cells were detected only at 8-12 weeks and their numbers generally increased thereafter. Permanent cell lines were established from a significant fraction of FV-P and FV-A-induced colonies, and these cell lines could be chemically induced to synthesize hemoglobin. All individual colonies produced complete Friend virus complex. However, virus production appeared to decline in at least some cell lines. Both FV-P- and FV-A-induced colonies contained cells capable of forming spleen colonies in irradiated recipients and subcutaneous tumors in unirradiated mice. Thus, the assay method described here appears to detect a unique class of malignant Friend virus-transformed cells that can be detected only in the advanced stages of Friend virus-induced erythroleukemia.

Animals↗

PubMed1979

Detection of gap junctions between the progeny of a canine macrophage colony-forming cell in vitro.

An in vitro monocyte-macrophage colony-forming cell (M-CFC) has been detected in canine bone marrow (BM). The colonies derived from these progenitor cells were similar to murine-derived M-CFC (MacVittie and Porvaznik, 1978, J. Cell Physiol. 97:305--314) colonies, since they showed a singular macrophage line of differentiation, a lag of 14--16 days before initiating colony formation, and they survived significantly longer in culture in the absence of colony-stimulating factor (CSF) than granulocyte-macrophage colony-forming cells (GM-CFC). Endotoxin (Salmonella typhosa lipopolysaccharide W)-stimulated dog serum was used as the CSF (7% vol/vol). Canine-derived M-CFC progeny were identified as macrophages on the basis of morphology, phagocytosis, and the presence of Fc receptors for IgG. Gap junctions were observed only in canine BM, M-CFC-derived colonies using freeze-fracture and lanthanum tracer techniques. They were not observed in any GM-CFC-derived colonies. The number of gap junctions observed in freeze-fracture replicas of BM, M-CFC-derived colonies (21 colonies from three different dogs) showed a significantly positive correlation (Kendall's tau = 0.70, P less than 0.001) with the size of the colony fracture plane area. Gap junctions were observed displaying hexagonal lattices of 9.3 nm +/- 0.08 (SE) particles with a center-to-center spacing of 10.4 nm +/- 1.0 (SE) on membrane P-fracture faces. On membrane E-fracture faces, highly ordered arrays of pits with 8.7 nm +/- 0.12 (SE) center-to-center spacing were observed. Arrays of both particles and pits were also observed in fracture-face breakthroughs within a gap junction. Thus, gap junctions can form in vitro between the cells of macrophage progeny of a canine M-CFC under appropriate growth conditions. The significance of this observation is that there may be a structural basis for cell-to-cell collaboration between BM macrophages and other capable cells that either pass into the tissue for modification or develop there into mature cell forms.

Animals↗

PubMed2002

Physiologic and pathologic consequences of granulocyte colony-stimulating factor deficiency.

Published studies have extended our understanding of granulocyte colony-stimulating factor deficiency. In granulocyte colony-stimulating factor withdrawal in humans, apoptosis seems to account for the dramatic loss of neutrophils, but whether the apoptosis results from normal cellular aging processes or accelerated cell loss upon granulocyte colony-stimulating factor withdrawal is unclear. In granulocyte colony-stimulating factor(-/-) mice, the introduction of bcl-2, an antiapoptotic gene product, did not affect the number of neutrophils in the circulation. This finding suggests that apoptosis does not account for the lack of neutrophils in this setting and that the reduction in neutrophil numbers in these mice results from processes other than the loss of large numbers of granulocyte colony-stimulating factor-dependent cells after commitment to the neutrophil lineage. In an experimental model of the induction of antigranulocyte colony-stimulating factor antibodies, the animals appeared remarkably similar to granulocyte colony-stimulating factor(-/-) mice. This finding confirms that at least some neutrophils are produced by granulocyte colony-stimulating factor-independent mechanisms and suggests that the antigranulocyte colony-stimulating factor antibodies reported in clinical studies before and after granulocyte colony-stimulating factor administration do not lead to similar consequences. A gross loss of neutrophils as seen in these granulocyte colony-stimulating factor-immune mice has never been reported in patients, suggesting that such an occurrence is unlikely to have occurred.

Animals↗

PubMed2003

Effect of granulocyte colony-stimulating factor on bleomycin-induced acute lung injury and pulmonary fibrosis.

OBJECTIVE: Potentially fatal pulmonary toxicity is a dreaded complication of bleomycin. Increased use of granulocyte colony-stimulating factor in patients receiving chemotherapy has been paralleled by an increased incidence of bleomycin-induced pulmonary toxicity. We investigated whether granulocyte colony-stimulating factor (25 microg x kg(-1) x day(-1), 4 days) enhanced endotracheal bleomycin-induced (5 mg/kg) acute lung injury and fibrosis in rats. SETTING: University laboratory. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: We compared the effects of alveolar instillation of bleomycin in rats treated with either granulocyte colony-stimulating factor or saline. MEASUREMENTS AND MAIN RESULTS: Mortality was 25% with bleomycin only and 50% with bleomycin + granulocyte colony-stimulating factor. Granulocyte colony-stimulating factor increased alveolar neutrophil recruitment, pulmonary edema, and lung myeloperoxidase activity on day 4. Lung static compliance on day 15 was severely decreased with bleomycin alone and showed a further significant decrease when granulocyte colony-stimulating factor was added (controls, 3.85 +/- 0.14 mL/kPa; bleomycin, 1.44 +/- 0.06 mL/kPa; and bleomycin + granulocyte colony-stimulating factor, 0.65 +/- 0.09 mL/kPa; control vs. bleomycin, p <.0001; and bleomycin vs. bleomycin + granulocyte colony-stimulating factor, p =.0003). Lung morphology with bleomycin + granulocyte colony-stimulating factor showed, in addition to the changes observed with bleomycin alone, four patterns indicating more severe disease: honeycomb foci, pleural thickening with hyaline fibrosis, interstitial granuloma with increased number of macrophages but not neutrophils, and established interstitial fibrosis. Lidocaine, which prevents neutrophil adhesion to endothelial cells, inhibited granulocyte colony-stimulating factor-related exacerbation of acute lung injury (bronchoalveolar lavage fluid cells and pulmonary edema) and pulmonary fibrosis (lung static compliance and morphologic changes). CONCLUSIONS: Granulocyte colony-stimulating factor enhances bleomycin-induced lung toxicity by a mechanism that probably involves neutrophils.

Animals↗

PubMed1979

Patterns of globin chain synthesis in erythroid colonies grown from sheep marrow of different developmental stages.

Erythroid colonies were grown from fetal sheep bone marrow at different stages of development and from adult marrow. Colony numbers increased with erythropoietin concentration, but fetal erythroid cells were more sensitive to the hormone than adult cells. Haemoglobin synthesis was characterized in the colonies and compared to that in control marrow incubations. No beta chain synthesis was detectable in marrow incubations or erythroid colonies from fetal marrow at 87-96 d gestation. Incubations of 115-120 d marrow shoed 5% beta chain synthesis while erythroid colonies synthesised up to 20% beta chains. Incubations and erythroid colonies from 125 d marrows showed about 27% beta chain synthesis, despite a similar increase in colony numbers with erythropoietin as the other marrows. Later in gestation, beta chain synthesis was lower in erythroid colonies than in marrow incubations and declined further in erythroid colonies as erythropoietin concentration increased. Adult marrow showed no detectable gamma chain synthesis but erythroid colonies produced up to 12% gamma chains, the identity of which was confirmed by peptide mapping. All changes in globin synthesis in vitro were correlated with colony numbers. In adult marrow, the maximal level of gamma chain production was inversely related to the cloning efficiency of the marrow samples studied. Potential uses of this model for studying globin gene expression are discussed.

Animals↗

PubMed1986

Effect of in vivo carcinogen exposure on colony formation and growth of hamster buccal pouch keratinocytes in culture.

The effect of in vivo carcinogen exposure on colony formation and growth of hamster buccal pouch keratinocytes in culture was evaluated at various times after exposing the mucosal surfaces of buccal pouches to initiating regimens of 7,12-dimethylbenz(a)anthracene (DMBA) or N-methyl-N-benzylnitrosamine (MBN). Keratinocytes were isolated by enzymatic dissociation of intact sheets of buccal pouch epithelium (HBPE) and separated into five fractions of varying buoyant density by isopycnic centrifugation through Percoll. The number of keratinocyte colonies which formed in cultures of unfractionated and fractionated HBPE was evaluated at 1, 2, 3, 4, and 8 weeks after treatment with DMBA and its control vehicle, paraffin oil, and at 6, 8, and 10 weeks after treatment with MBN and its control vehicle, propylene glycol. The rate of colony growth expressed as population doublings per day was determined at these same time periods in unfractionated cultures of carcinogen and control treated HBPE. Unfractionated control (paraffin oil and propylene glycol) cultures gave rise to a uniform number of keratinocyte colonies with a growth rate of approximately 1 population doubling per day at each time period examined. Control cultures of fractionated HBPE exhibited considerable variation in their capacity to form keratinocyte colonies. Fraction 5 cultures which were composed almost exclusively of basaloid cells failed to form colonies. Cultures of unfractionated and fractionated DMBA and MBN-treated HBPE exhibited a marked and persistent suppression in the number and growth of keratinocyte colonies. In addition we observed the development of a morphologically unique type of keratinocyte colony that first emerged in the high density, basaloid-rich fraction 5 cultures, and which subsequently developed in all fractionated and unfractionated HBPE cultures. These unique keratinocyte colonies were never observed in control cultures. These results demonstrate that in vivo exposure of HBPE to DMBA or MBN causes a marked and prolonged suppression in the number and growth of keratinocytes colonies in culture. Furthermore the treatment regimens appeared to induce or select for a population of keratinocytes which persisted in vivo and which exhibited a unique colony morphology when grown in surface culture.

Animals↗

PubMed1987

Survival of highly proliferative colony forming cells after treatment of bone marrow cells with 4-hydroperoxycyclophosphamide.

We investigated the in vitro effects of 4-hydroperoxycyclophosphamide (4-HC) on human hemopoietic stem cells. Marrow cells were exposed to 4-HC and then assayed for mixed (CFU-GEMM), erythroid (BFU-E), megakaryocyte (CFU-M), and granulocyte-macrophage (CFU-GM) colony forming cells. We found that highly proliferative colony forming cells, especially CFU-GEMM and BFU-E, were relatively spared by 4-HC treatment. One third of the surviving progenitors formed large colonies, some of which contained more than 50,000 cells. By sequential examination of the formation of these large colonies, we found immature colonies consisting of blasts at the early stage of culture. The morphology of these "blast cell colonies" in situ was arbitrarily classified into four types. Among them were the blast cell colonies consisting of the individual cells that were dispersed and had a few granules within the cytoplasm (type A); these cells finally formed very large colonies on day 22 of culture. Approximately 70% of the single cells derived from type A blast cell colonies produced secondary colonies consisting of erythroblasts, macrophages, eosinophils, and/or basophils. These results show that the blast cells in type A colonies have a highly proliferative capacity. The availability of a highly enriched population of primitive hemopoietic progenitors will provide us with a unique opportunity to study the interaction between a single stem cell and purified hemopoietic factors.

Bone Marrow Cells↗

PubMed1980

In vitro immune response of human peripheral lymphocytes. VI. Distribution and characterization of precursors for PHA- and protein A-induced colony-forming B cells.

B cells from peripheral blood or cord blood formed colonies by stimulation with either PHA or protein A. On the other hand, tonsillar B cells did not form protein A-induced colonies, although PHA-induced colony formation was comparable to that observed in peripheral B cells. Lack of protein A-induced colony formation in tonsillar B cells was not due to the defect of helper T cells in preculture or to the presence of suppressor cells but was due to the absence of precursors for colony formation. The result showed that PHA- and protein A-induced colony-forming cells belonged to distinct subsets of B cells. Depletion of mu-bearing cells from peripheral B cells abrogated both PHA- and protein A-induced colony formation. Depletion of delta-bearing cells did not affect PHA- and protein A-induced colony formation and the population enriched with delta-bearing cells also showed colony formation. Depletion of complement receptor (CR)-positive cells removed precursors for both PHA- and protein A-induced colony formation. These results showed that precursor cells for PHA- and protein A-induced colony formation were IgM+, IgD+ and CR+ or IgM+, IgD- and CR+.

Animals↗

PubMed2002

Rat granulocyte colony-forming unit (CFU-G) assay for the assessment of drug-induced hematotoxicity.

To assess the drug-induced hematotoxicity to granulocyte progenitors, we established a modified colony-forming assay using rat bone marrow cells (BMCs). In the presence of various colony-stimulating factors (CSFs), rat BMCs were disseminated on methylcellulose at a concentration of 1.3 x 10(4) cells/cm(2) (5 x 10(4) cells/0.5 ml/well in a 12-well plate). Mouse granulocyte-macrophage colony-stimulating factor (mGM-CSF) stimulated the formation of almost all macrophage colonies. Human granulocyte colony-stimulating factor (hG-CSF) alone or in combination with mouse interleukin-3 (mIL-3) did not significantly effect on the number of rat colony-forming units in culture (CFU-C). When BMCs were seeded at 5.2 x 10(4) cells/cm(2) (5 x 10(5) cells/1 ml/dish in a 35-mm dish), hG-CSF increased the number of the colonies in a dose-dependent manner, and resulted in about 50 colonies at 50 ng/ml. The constituent cells of the colonies were identified as neutrophils. Under these conditions, the effects of 5-fluorouracil (5-FU) on granulocyte colony-forming units (CFU-G) were examined in rats and mice. The inhibitory effect of 5-FU on rat CFU-G was similar to the effect on mouse CFU-G. These results indicate that the rat CFU-G induced by hG-CSF is capable of being used for the evaluation of drug-induced hematotoxicity.

Animals↗

PubMed1990

The effects of interleukin-3, GM-CSF, and G-CSF on the growth kinetics of colony-forming cells in myelodysplastic syndromes.

In order to obtain more insight into the nature of the abnormal in vitro colony formation in myelodysplastic syndromes (MDS), we investigated the kinetics of the colony formation of 23 MDS cases in response to recombinant human interleukin-3 (IL-3), Granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating Factor (G-CSF), and giant cell tumor cell line conditioned medium (GCT-CM). The kinetics of GCT-CM-induced colony formation were comparable to that of G-CSF-induced colony growth, both in MDS and in normal bone marrow cultures. Colony formation was found to be delayed in MDS. The delay in colony formation was most apparent in the GCT-CM (G-CSF) responsive progenitor cell compartment. In MDS cases with clinical features of high risk disease, this delay was more pronounced as compared with low risk cases (7 and 3 days, respectively, in response to GCT-CM). The delay in colony formation was found to be caused by an increase in the time interval before progenitor cells had begun to divide. These results suggest that a prolongation of the time spent in G0 of myeloid progenitor cells in MDS may be the cause of the indolent in vitro colony formation observed in this disease.

Bone Marrow↗

PubMed1988

Synergistic interactions between hematopoietic growth factors as detected by in vitro mouse bone marrow colony formation.

We have investigated the proliferative effects of several combinations of hematopoietic growth factors in agar cultures of murine bone marrow cells. Granulocyte-macrophage colony-stimulating factor (GM-CSF) synergized with granulocyte colony-stimulating factor (G-CSF), while G-CSF also synergized with macrophage colony-stimulating factor (CSF-1) and interleukin 3 (IL3), resulting in colony numbers greater than the sum of the numbers of colonies formed with each factor alone. In addition, these combinations resulted in increased colony sizes, with the formation of day-14 colonies with diameters greater than 0.5 mm. The combination of GM-CSF plus IL3 showed an increase in numbers of colonies that approximated the sum of that seen with each factor alone, however, the size of the colonies was increased with a number of day-14 and day-21 colonies having diameters greater than 0.5 mm. These data add to the list of hematopoietic factors known to synergistically stimulate myeloid progenitors and suggest that some of these interactions may be on early progenitor cells with high proliferative potentials.

Animals↗

PubMed1975

Heterogeneity of in vitro colony- and cluster-forming cells in the mouse marrow: segregation by velocity sedimentation.

C57BL bone marrow cells were separated on the basis of their sedimentation velocity at unit gravity and cell fractions cultured in agar using three types of colony stimulating factor (CSF). Colony-forming cells separated as a single peak (s equal 4.4 mm/hr) in cultures stimulated by mouse lung conditioned medium (CSFMLCM) or endotoxin serum (CSFES). Cluster-forming cells were separable into two peaks and the majority were larger than colony-forming cells (s equal 5.7 mm/hr). Partial segregation of colony-forming cells was observed according to the morphological types of colonies generated, large cells tending to generate macrophage colonies and small cells, granulocytic colonies. Large colony-forming cells were more responsive to stimulation by CSF than small cells. Human urine (CSFHU) appeared unable to proliferation of most small colony-forming cells. Colony-forming cells appear to be a highly heterogeneous population with intrinsic differences in responsiveness to CSF and with differing capacities to generate colonies whose cells differentiate to granulocytes of macrophages.

Animals↗