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At least 199 records · Page 11Linked to original sources
PubMed1994

Induction of granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) expression in bone marrow and fractionated marrow cell populations by interleukin 3 (IL-3): IL-3-mediated positive feedback mechanisms of granulopoiesis.

Interleukin 3 (IL-3) induces proliferation and differentiation of mast cell progenitors in vitro, whereas it induces granulocytosis in vivo. In this paper, a positive feedback mechanism of granulopoiesis was studied in order to elucidate the granulocytosis induced by IL-3 in mouse. IL-3 induced expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in total bone marrow cells and a marrow adherent cell population. In fractionated marrow cell populations, a different expression pattern of induction of IL-3 stimulation was observed; GM-CSF was expressed in macrophages and fraction 1 (P < 1.061) and 2(1.061 < P 1.074) of bone marrow cells fractionated by equilibrium density centrifugation, G-CSF was expressed in macrophages and fraction 2 and 3 (1.074 < P < 1.097), and interleukin 6 (IL-6) in macrophages and fraction 1 to 3. These results indicate a hierarchical regulation of cytokine production and the existence of a positive feedback mechanism in granulopoiesis. IL-6, induced by IL-3, stimulates stem cells into cycle and induces stem cells to respond to IL-3. The stem cells differentiate to granulocyte-macrophage colony-forming cells by the combined effect of IL-3 and IL-6. IL-3 also induces GM- and G-CSF expression which in turn makes granulocyte-macrophage colony-forming cells differentiate to granulocytes. These factors organize a cytokine network in granulopoiesis.

Animals↗
PubMed1996

Expression of granulocyte colony-stimulating factor and granulocyte colony-stimulating factor receptor genes in partially overlapping monoclonal B-cell populations from chronic lymphocytic leukemia patients.

B lymphocytes were purified from the peripheral blood of 30 B-cell chronic lymphocytic leukemia (B-CLL) patients and tested for the ability to produce granulocyte colony-stimulating factor (G-CSF) in vitro. Fifteen Staphylococcus aureus Cowan I (SAC)-stimulated, but not unstimulated, B-cell suspensions produced G-CSF in short-term cultures. Accordingly, G-CSF mRNA was detected only in SAC-stimulated B cells. Five CLL B-cell fractions that released G-CSF following exposure to SAC were also incubated with CD40 or anti-mu antibodies in the presence or absence of recombinant (r) interleukin-2 (IL-2) or IL-4. The 5 cell suspensions produced G-CSF only on culture with CD40 monoclonal antibody in combination with rIL-2 or rIL-4. CD5+ B lymphocytes, which represent the normal counterparts of most B-CLL proliferations, did not produce G-CSF under any of the above culture conditions. G-CSF produced by leukemic B lymphocytes was biologically active, because conditioned media of SAC-stimulated cells supported the in vitro growth of myeloid colonies from normal bone marrow progenitors. The colony stimulating activity of CLL B-cell supernatants was ascribed to both G-CSF and granulocyte-macrophage colony stimulating factor. G-CSF receptors (G-CSFRs) were detected on freshly isolated B lymphocytes from 7 of 11 B-CLL patients; 5 of these cell suspensions produced G-CSF in culture, whereas 2 did not. rG-CSF rescued 3 of the 7 G-CSFR+ cell fractions from spontaneous apoptosis but had no effect on their in vitro proliferation.

B-Lymphocytes↗
PubMed1998

Human CD34(+) bone marrow cells regulate stromal production of interleukin-6 and granulocyte colony-stimulating factor and increase the colony-stimulating activity of stroma.

Cytokines produced by stromal cells induce the proliferation and differentiation of hematopoietic cells in the marrow microenvironment. We hypothesized that cross-talk between hematopoietic cells at different stages of differentiation and stromal cells influences stromal cytokine production and is responsible for maintaining steady-state hematopoiesis and responding to stress situations. We show that coculture of primitive CD34(+) cells in contact with or separated by a transwell membrane from irradiated human bone marrow stromal layers induces a fourfold to fivefold increase in interleukin-6 (IL-6) and granulocyte colony-stimulating factor (G-CSF) levels in the stromal supernatant (SN) during the first week. Levels of both cytokines decreased to baseline after coculture of CD34(+) cells for 3 to 5 weeks. Coculture of more mature CD15(+)/CD14(-) myeloid precursors induced only a transient 1.5- to 2-fold increase in IL-6 and G-CSF at 48 hours. Neither CD34(+) nor CD15(+)/CD14(-) cells produced IL-6, G-CSF, IL-1beta, or tumor necrosis factor alpha. When CD34(+) cells were cultured in methylcellulose medium supplemented with cytokines at concentrations found in stromal SN or supplemented with stromal SN, a fourfold to fivefold increase in colony formation was seen over cultures supplemented with erythropoietin (EPO) only. When cultures were supplemented with the increased concentrations of IL-6 and G-CSF detected in cocultures of stroma and CD34(+) cells or when CD34(+) cells were cocultured in methylcellulose medium in a transwell above a stromal layer, a further increase in the number and size of colonies was seen. The colony-forming unit-granulocyte-macrophage-stimulating activity of stromal SN was neutralized by antibodies against G-CSF or IL-6. These studies indicate that primitive CD34(+) progenitors provide a soluble positive feedback signal to induce cytokine production by stromal cells and that the observed increase in cytokine levels is biologically relevant.

Antigens, CD34↗
PubMed1992

Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF): receptor biology, signal transduction, and neutrophil activation.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) are two of the growing number of recognized cytokines involved in the regulation of hematopoiesis. The purification of these factors and the subsequent cloning of the cDNAs which encode these proteins have led to their widespread clinical use in the setting of therapy or disease-induced myelosuppression. Although originally purified on the basis of their colony-stimulating properties, GM-CSF and G-CSF may also play important roles in the regulation of effector cell function. The mechanisms underlying progenitor cell proliferation and effector cell stimulation remain poorly understood. However, the characterization of the GM-CSF and G-CSF receptors and recent work in signal transduction are helping to elucidate these mechanisms. This paper will review the biology of the GM-CSF and G-CSF receptors, the mechanisms of post-receptor signal transduction, and the resultant effects on neutrophil function. In addition, the current and potential clinical uses of these factors will be examined in light of their ability to activate and perhaps enhance the function of neutrophils.

Animals↗
PubMed1992

Acute arterial thrombosis after escalated-dose methotrexate, vinblastine, doxorubicin, and cisplatin chemotherapy with recombinant granulocyte colony-stimulating factor. A possible new recombinant granulocyte colony-stimulating factor toxicity.

Combination chemotherapy with a regimen of methotrexate, vinblastine, doxorubicin, and cisplatin (M-VAC) has produced long-term survival times in a significant proportion of patients with advanced nodal and metastatic urothelial tumors. The availability of the colony-stimulating factors has spurred interest in studies evaluating escalated dosing schedules of M-VAC in an attempt to improve major response rates and overall survival. More frequent use of the colony-stimulating factors, however, in this and other settings may be associated with unrecognized side effects. The authors report a case of arterial thrombosis in a 69-year-old man receiving recombinant granulocyte colony-stimulating factor (rhG-CSF) and escalated-dose M-VAC for treatment of a transitional cell carcinoma of the bladder. Incidents of venous thrombosis have been reported previously with the use of colony-stimulating factors, but, to the knowledge of the authors, this case represents the first report of an arterial thrombosis occurring in a patient receiving rhG-CSF.

Aged↗
PubMed1985

Evaluation of colony-forming ability experiments using normal and DNA repair-deficient human fibroblast strains and an automatic colony counter.

An automated procedure for evaluation of colony-forming ability experiments has been developed using normal and xeroderma pigmentosum fibroblast strains. Technically this consists of an image analyzer equipped with a contrast-intensifying video camera, monitor, and a desk-top computer. Complex structures composed of overlapping colonies could be reduced to the constituent single colonies by special correction programs. Eighteen experiments were evaluated, and the D0 values for colony-forming ability were determined. A systematic but correctable deviation between visual and automated counting was found. The source of this deviation is described and a solution for correction is provided. The automatic procedure reduced the evaluating time by a factor of five to ten.

Cell Count↗
PubMed1986

VH gene family utilization in colonies derived from B and pre-B cells detected by the RNA colony blot assay.

The immunoglobulin heavy chain variable region (VH) genes of the mouse have been categorized into families based upon sequence homology. Utilizing the RNA colony blot assay we have determined the expression of eight of these families in B cell colonies derived from either surface immunoglobulin positive (sIg+) adult spleen B cells or sIg- fetal liver pre-B cells. We demonstrate, based upon the analysis of greater than 6000 individual colonies, that VH gene usage is a characteristic of the mouse strain studied. C57BL/6 mice most frequently (45%) utilize family VHJ558, the largest VH family, whereas BALB/c mice most frequently (22%) utilize family VH7183, the most JH proximal family in BALB/c mice. Moreover, colonies derived from sIg- fetal liver derived precursors show similar patterns, suggesting that selection based on exogenous antigen is not an important parameter in determining VH gene family usage.

Animals↗
PubMed1985

Soft agarose culture human tumour colony forming assay for drug sensitivity testing: [3H]-thymidine incorporation vs colony counting.

In vitro drug sensitivity testing, both by optical colony counting and by a [3H]-TdR incorporation assay, was performed on human tumour cells proliferating in soft agar cultures. Cells from two different human tumour cell lines, 5 different human tumour xenografts, and 94 different primary human tumour specimens of various histologic types were studied. Regression analysis comparing the results of the colony counting assay and the [3H]-TdR assay revealed good to excellent correlations between the two assay endpoints for quantitating the effect of in vitro anticancer drug exposure for a large number of different agents. The presence of pre-existing tumour cell aggregates complicates the performance of the optical colony counting assay. The [3H]-TdR incorporation assay is more sensitive and reproducible than the colony counting assay when performed on samples containing a large number of initially seeded tumour cell aggregates.

Antineoplastic Agents↗
PubMed1979

Cyclic hematopoiesis. Effects of endotoxin on colony-forming cells and colony-stimulating activity in grey collie dogs.

Cyclic changes in blood neutrophil counts of grey collie dogs with cyclic hematopoiesis can be eliminated by daily endotoxin injections. Studies were performed to determine the mechanism whereby endotoxin alters this disease. Bone marrow granulocyte-macrophage progenitor cells (colony-forming cells [CFUc]) showed cyclic variation in the untreated grey collie, which was eliminated by chronic endotoxin treatment (Salmonella typhosa lipopolysaccharide W, 5 microgram/kg per day). Similar cyclic variation in blood CFUc was eliminated by this treatment. Tritiated thymidine suicide of the marrow colony-forming cells failed to show cyclic changes to explain the marked swing in CFUc numbers in untreated grey collies. The thymidine suicide rates were not significantly changed by chronic endotoxin treatment. Similarly, serum colony-stimulating activity did not show cyclic variation with the cyclic neutrophil counts in untreated grey collies and was not altered by chronic endotoxin treatment. We suggest that endotoxin eliminates neutrophil cycling in cyclic hematopoiesis by a direct effect on the flux of pluripotent stem cells into the committed stem cell compartment and that this occurs independent of changes in serum colony-stimulating activity.

Animals↗
PubMed1976

Relationship of colony-stimulating activity to apparent kill of human colony-forming cells by irradiation and hydroxyurea.

Suspensions of human bone marrow cells were subjected to 137Cs irradiation in vitro and then cultured in semisolid agar medium. Cultures of irradiated cells were stimulated with colony-stimulating activity (CSA) of different potencies, and it was found that the amount of stimulation applied to cultures influenced the apparent kill of colony-forming cells (CFC). It was also found that the effects of irradiation on colony formation were not confined to CFC kill since medium conditioned by cells during irradiation exhibited stimulatory and inhibitory properties after treatment by 600 and 1000 rads, respectively. Studies in which irradiated cells were pretreated with hydroxyurea indicated that CFC in the DNA synthetic phase of the cell cycle were particularly sensitive to low doses of irradiation. The proliferative capacity of CFC surviving 1000 rads was undiminished as judged by their ability to form large colonies. Estimates of CFC kill by hydroxyurea were also affected by the level of CSA.

Bone Marrow↗
PubMed1992

Brain microvascular smooth muscle and endothelial cells produce granulocyte macrophage colony-stimulating factor and support colony formation of granulocyte-macrophage-like cells.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a potent stimulator of macrophages and neutrophils and plays a role in inflammatory diseases. In this article, we report that mouse brain-derived microvascular smooth muscle cells (SM) and endothelial cells (En) in coculture with splenocytes support the colony proliferation of immature granulocyte-macrophage-like (GM) cells. Unstimulated SM and En cells release GM-CSF as shown by ELISA assay and SM expresses mRNA for GM-CSF by polymerase chain reaction (PCR). Stimulation of SM and En by a nonspecific activator (lipopolysaccharide) results in upregulation of GM-CSF production. GM colonies cannot be grown on cultured astrocytes or on extracellular matrix alone prepared from smooth muscle or endothelium. However, colonies form on the extracellular matrix and on astrocytes, either in the presence of SM- or En-conditioned medium or after the addition of recombinant GM-CSF. The GM cells are positive for nonspecific esterase, peroxidase, and MAC-1 markers but are negative for FC gamma receptors and for Thy 1.2, CD8, CD4, MHC class II, and Asialo GM1 markers. These observations emphasize the possibility for active participation of brain microvasculature SM and En in acute inflammatory reactions of the central nervous system.

Amino Acid Sequence↗
PubMed1978

Specific antibody-forming B-lymphocyte colonies. I. Distribution and nature of SRBC antibody-forming B-lymphocyte colonies in mouse lyphomyeloid organs.

Wehn normal mouse spleen or lymph node cells are cultured for 7 days in agar-medium containing 2-mercaptoethanol and sheep red blood cells (SRBC), approximately one B lymphocyte colony (BLC) develops per 50-100 cells seeded. Incubation of cultures for 3 h with guinea-pig complement at day 7, demonstrated that 0.05-0.25% of all BLC form specific antibody against SRBC (SRBC-AF-BLC). The SRBC specific colonies appear centrally in lytic plaques of 2-5 mm in diameter and cells recovered from individual SRBC-AF-BLC were shown to produce antibodies of the IgM class against SRBC. Cells forming SRBC-AF-BLC are absent in the new-born and infantile spleen but appear in adult mice with a frequency of 5, 10-25 and 25-70 per 10(6) bone marrow, spleen and lymph node cells respectively. specific immunization in vivo or in vitro does not greatly affect the number of SRBC-AF-BLC-forming cells. Cytolysis of spleen cells with anti-Ig serum plus complement prior to culture reduced the number of total BLC and that of specific SRBC-AF-BLC by 93% and 94% respectively. The peak sedimentation velocity of both SRBC-AF-BLC-forming cells and total BLC-forming cells was 3.5 mm/h. Spleen cells enriched 200-300 times for cells that bind specifically to the hapten NIP were not enriched for cells forming colonies with specific antibody production against NIP. The data indicate that the cells that give rise to specific antibody-forming colonies belong to a mature virgin B cell group of small Ig-positive B lymphocytes.

Age Factors↗
PubMed1985

Human colony-stimulating activity-producing tumor: production of very low mouse-active colony-stimulating activity and induction of marked granulocytosis in mice.

We reported previously a human lung cancer which induced marked granulocytosis both in the patient and in the tumor-transplanted nude mice (G-1 mice), and whose conditioned media (G-1-T-CM) contained both human-active colony-stimulating activity (h-CSA) (810 colonies/ml) and mouse-active colony-stimulating activity (m-CSA) (530 colonies/ml), suggesting that the CSA produced by the tumor caused granulocytosis both in the patient and in G-1-mice. We reported here another human lung cancer which induced marked granulocytosis both in the patient and in the tumor-transplanted nude mice (G-2-mice). However, in contrast to the tumor reported by us previously, the conditioned media of this tumor (G-2-T-CM) contained only very weak m-CSA (86 colonies/ml), although h-CSA was very strong (7332 colonies/ml). The ratio of m-CSA to h-CSA in G-1-T-CM (0.654) was 55-fold higher than that in G-2-T-CM (0.012). Gel filtration of G-2-T-CM on a Sephadex G-150 column denied the presence of colony-inhibiting activity which inhibited m-CSA in G-2-T-CM. Since the addition of serum obtained from G-2 mice did not enhance m-CSA in G-2-T-CM, it seems unlikely that the G-2 tumor produced an inactive form of m-CSA which was activated in G-2 mouse serum. G-2-T-CM tended to maintain the number of colony-forming units in spleen in mouse bone marrow during liquid cultures, while G-1-T-CM did not. These results may indicate that the G-2 tumor produced a humoral factor which has very weak CSA and acts on stem cells rather than on committed progenitors.

Animals↗
PubMed1977

[Stimulation of the growth of murine bone marrow colonies in vitro by an acute inflammatory exudate. Comparison with colony stimulating factor CSF)].

Formation of colonies from mice bone marrow progenitors of macrophages and granulocytes in methylcellulose culture was induced by an inflammatory pleural exudate obtained from mice injected with dextran. Mitogenic activity of this acute inflammatory exudate was compared with that of colony stimulating factor (CSF). It was found that colony and cluster counts, during 10 days of culture, were similar with the two types of stimulating factors. When used at the same dose, exudate was less active than CSF. It was concluded that inflammatory exudate showed an activity similar to that of CSF but contained a smaller amount of stimulating factor. Further cytochemical studies are necessary to specify whether or not the two factors induced the same type of colonies (monocytic or granulocytic).

Animals↗
PubMed1979

Bacillus Calmette-Guérin enhancement of colony-stimulating activity and myeloid colony formation following administration of cyclophosphamide.

Pretreatment of mice with Bacillus Calmette-Guérin (BCG) enhances recovery of the peripheral granulocyte count from cyclophosphamide (CTX)-induced leukopenia. In the present study, in vitro bone marrow culture was used to assess the effect of BCG pretreatment on serum levels of myeloid colony-stimulating activity and on regeneration of bone marrow myeloid colony-forming units (CFU-c) following CTX. C57BL/6 mice received either BCG or 0.9% NaCl solution i.p. 8 days prior to the administration of CTX (300 mg/kg i.p.). Following CTX, peak serum levels of myeloid colony-stimulating activity were strikingly higher in the BCG-pretreated mice [1320 +/- 30 (S.E.) units] than in the 0.9% NaCl solution-pretreated mice (764 +/- 37 units). BCG pretreatment also resulted in higher numbers of marrow CFU-c during recovery from CTX (e.g., 43.9 +/- 1.8 versus 20.0 +/- 0.9 myeloid colonies/10(5) marrow cells, Day 3 post-CTX). However, neither the rate of decline nor the absolute nadir of CFU-c, nor CFU-c cell cycle characteristics were affected by the pretreatment. The initial effect of i.p. BCG pretreatment on recovery from CTX-induced granulocytopenia is an augmentation of serum myeloid colony-stimulating activity which precedes the enhanced regeneration of CFU-c and the accelerated recovery of the peripheral granulocyte count.

Animals↗
PubMed1981

Colony formation by bone marrow cells after incubation with neuraminidase. III. Cell surface repair, homing and growth characteristics of colony forming cells in vivo.

Incubation of bone marrow cells (BMC) with neuraminidase (NA) reduced their ability to form colonies in the spleen of lethally irradiated mice to 25% of control-incubated BMC. Covering of the recipient's receptors for galactosyl residues by infusion of desialated erythrocyte membrane fragments (NA-Efr) fully prevented the reduction of NA-BMC colony formation. Upon retransplantation the desialated CFUS in the spleen of irradiated first recipients could be significantly rescued within 6 h posttransplantation by NA-Efr treatment of secondary recipients. Transplantation experiments, including NA-Efr infused and normal primary and secondary recipients, indicated that repair of the desialated CFUS cell surface probable occurred within 48 h. Establishment of growth curves indicated that desialation of CFUS did not alter their proliferative capacity but probable retarded the cells to proliferate in normal irradiated recipients for about 24 h. This might be the cause of the decreased CFUS content observed in the first recipients' spleen colonies. This delay in the onset of proliferation was not observed in mice with covered galactosyl receptors. The present experiments further indicate that (a) injected desialated CFUS are rapidly sequestrated in the recipient's body; (b) more desialated CFUS initially seed into the spleen than actually form colonies; (c) the spleen probably contains D-Galactose-specific receptors; (d) CFUS may largely restore their surface properties within 24 h following desialation, and (e) the organ distribution of normal CFUS is changed upon injection in NA-Efr infused recipients. Experiments with 51Cr-tagged BMC suggested that the organ distribution of BMC was similarly affected by neuraminidase treatment as that of CFUS.

Animals↗
PubMed1984

The role of erythropoietin, thrombopoietic stimulating factor, and myeloid colony-stimulating factors on murine megakaryocyte colony formation.

Various growth factors including purified erythropoietin, colony-stimulating factor (CSF-1), and granulocyte-macrophage CSF (GM-CSF) were tested for their ability to stimulate megakaryocytopoiesis. Four separate preparations of erythropoietin were tested in highly defined cell culture medium. One unit of purified material stimulated small but significant numbers of megakaryocyte colonies, both in serum-containing and in serum-free cultures. All other erythropoietin preparations failed to induce megakaryocyte colony formation. Purified erythropoietin showed no synergistic activity with either WEHI-3 cell conditioned medium (WEHI-3CM, a source of both megakaryocyte CSF and megakaryocyte-potentiating activity) or P388D1 cell conditioned medium (P388D1CM, a preparation containing megakaryocyte potentiator). Partially purified thrombopoietic stimulatory factor did not stimulate directly megakaryocyte colony formation, but acted together with WEHI-3CM, augmenting the number of clonable progenitors detected. Optimal activity was observed at 12-25 micrograms protein per plate. Myeloid growth factors (CSF-1 and GM-CSF) were inactive in the murine megakaryocyte assay. The data show lineage specificity for the myeloid stimulators, but a purified erythropoietin preparation was found to stimulate a small level of megakaryocytopoiesis.

Animals↗
PubMed1997

High-dose granulocyte-colony stimulating factor (G-CSF) in vitro induces the growth of high proliferative potential colony forming cells (HPP-CFC) in patients undergoing blood stem cell mobilization.

We evaluated the role of high-dose granulocyte colony stimulating factor (G-CSF) in vitro, in inducing the generation of high-proliferative potential colony forming cells (HPP-CFC), from either mononuclear cells or purified CD34+ cells. Both normal controls and patients undergoing peripheral blood stem cell (PBSC) mobilization and transplantation were studied. In serum-driven agar cultures, G-CSF stimulated the proliferation of HPP-CFC in a dose dependent manner (r = 0.92). The number of HPP-CFC was four-fold greater in mobilized patients than in normal controls. Purified CD34+ cells yielded 11-fold more colonies than mononuclear cells. HPP-CFC from mobilized patients showed replating capacity, giving rise to secondary colonies of more mature appearance. In serum-free cultures, the effect of G-CSF appeared to be mediated by synergistic interaction with stem cell factor. Our results suggest that G-CSF stimulates primitive hematopoietic cells that are detectable in increased amounts in patients receiving mobilization therapy. Therefore, determination of G-CSF induced HPP-CFC could be a useful tool in the evaluation of mobilization strategies.

Antigens, CD34↗