Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Granulocyte Precursor Cells”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Effects of myeloproliferative sarcoma virus on the pluripotential stem cell and granulocyte precursor cell populations of DBA/2 mice.

The hematopoietic stem cell (CFU-S) and granulocyte precursor cell (CFU-C) populations have been assayed in the spleen, blood, and bone marrow of DBA/2 mice at various times after infection with the myeloproliferative sarcoma virus (MPSV). Beginning between 7 and 19 days after virus infection, the number of CFU-S showed a steady, parallel increase in the blood and spleen, reaching a maximum at both sites by days 25-30. At the maximum, in the spleen the concentration of CFU-S was 10 times greater than that in the blood, and the total number of CFU-S was over 100 times greater than that of normal animals. During the same period, in the bone marrow the number of CFU-S decreased to one-half of normal. Nevertheless, the CFU-S from MPSV-infected animals differentiated normally in the spleens of irradiated, normal recipient mice (except for some hyperplasia of the erythroid component of spleen colonies). The CFU-C content of the bone marrow, spleen, and blood paralleled the CFU-S content of these organs: The CFU-S and CFU-C populations changed almost synchronously after MPSV infection. In the terminal stage of the MPSV-induced disease, a variable proportion of the CFU-C population acquired the ability to differentiate in the absence of added colony-stimulating factor.

Animals↗

Factors produced by macrophages and tumor cells: influence on the granulocytic precursor cells (CFU-C) in normal and tumor-bearing mice.

Some tumors are known to produce colony-stimulating factors (CSF). In mice bearing s.c. Ehrlich tumor (ET) we observed that tumor growth is responsible for hemopoietic perturbations in which the increase of granulocytic-macrophagic precursors (CFU-C) in bone marrow and in the spleen represents a remarkable aspect. CFU-C in bone marrow from ET-bearing mice are more sensitive than CFU-C from normal mice to CSF from L-cells (LC-CM), mouse embryo fibroblasts (MEF-CM) and from the same tumor (ET-CM). Macrophages from normal and from ET-bearing mice exert the same effect on the proliferation of normal bone marrow CFU-C. Bone marrow CFU-C from ET-bearing mice show an increased sensitivity to the inhibitory factors produced by macrophages from ET-bearing mice.

Animals↗

Electronic sorting of granulocyte precursor cells from stimulated bone marrow.

A commerical cell sorter was used to obtain preparations of cells in various stages of granulocyte development from rabbit marrows stimulated by inflammatory response. Marrow cells were fractionated on density gradients of Ficoll/Hypaque and each fraction sorted using light scatter. Trial and error selection of appropriate gradient fractions and light scatter windows allowed sorting of early (blast cells, promyelocytes), intermediate (myelocytes, metamyelocytes) and late stage (band cells, polys) granulocytes with enhanced purity.

Animals↗

Anti-thymocyte globulin effective in the treatment of aplastic anemia does not stimulate granulocyte precursor cells.

To find out whether the preparations of anti-lymphocyte or anti-thymocyte globulin (ATG), successfully used in our center for the treatment of patients with aplastic anemia, were stimulatory for hematopoietic precursor cells, we studied the effect on CFUC in 30 normal bone marrow samples. Although in 2 out of 30 cases stimulation was observed, the overall result for both the horse anti-lymphocyte globulin and the rabbit anti-thymocyte globulin was dose-dependent and complement-dependent inhibition. Neither in the absence, nor in the presence of complement was there any indication of consistent stimulation of CFUC. When bone marrow was depleted of E-rosette forming cells, the incubation of the depleted fraction with ATG did not result in stimulation. The incubation of the E-rosette positive fraction with ATG, followed by the addition of these treated cells to untreated E-rosette depleted cells was equally ineffective in giving any stimulation of CFUC. Our data suggest that the effect of ATG in the treatment of aplastic anemia is not due to direct stimulation of hematopoietic precursor cells.

Anemia, Aplastic↗

Effect of peripheral blood lymphocytes from systemic lupus erythematosus patients on human bone marrow granulocyte precursor cells (colony-forming units in culture).

Because of the possibility that immunological mechanisms might be involved in the pathogenesis of leukopenia accompanying systemic lupus erythematosus (SLE), the effect of lymphocytes on colony-forming units in culture (CFU-C) was compared. The colony formation of the bone marrow CFU-C of SLE patients was less than that of the healthy subjects. Lymphocytes of SLE patients and serum of some of the SLE patients remarkably inhibited colony formation by human bone marrow CFU-C. The results shown above suggest the possibility that immunocompetent cells of the patients are involved in the pathogenesis of leukopenia in SLE.

Adolescent↗

Granulocyte precursor cell studies in Schistosoma mansoni patients with eosinophilia.

Eosinophilia is a common clinical presentation in patients with helminthic infections. A study was designed to determine the mechanism(s) for selective or preferential differentiation of precursor cells into mature eosinophils (eos). Thus, experiments were performed to delineate the frequency of colony forming units of eos (CFU-eos) in the peripheral blood of Egyptian patients with active Schistosoma mansoni infection with eosinophilia and normal healthy individuals. The number of CFU-eos among the nonadherent mononuclear cell population was assessed in a double layer soft agar culture with autologous unfractionated mononuclear cells serving as a source of colony stimulating factor(s). Following 14 days of incubation, discrete colonies were distinguished morphologically as eosinophilic, neutrophilic, or mixed. Results indicated a two-fold increase in the total number of colonies per 10(6) cultured nonadherent cells in patients with S. mansoni infection when compared to the number of colonies obtained with adult normal volunteers (57 +/- 10 vs. 24 +/- 4; P less than 0.025). However, the frequency of CFU-eos and CFU-neut was similar in patients and normal individuals (66 +/- 3 vs. 59 +/- 8 percent CFU-eos; 30 +/- 4 vs. 35 +/- 6 percent CFU-neut). These data suggest that: eosinophils may differentiate from progenitor cells at other anatomical sites; there may be an increase in the half life of mature eosinophils in patients; there is no strict correlation between the frequency of progenitor cells and the number of differentiating mature cells of this lineage at least as measured by this in vitro assay; and the in vitro assay may not quantitatively reflect the in vivo differentiating capacity of progenitor cells.

Adolescent↗

Enhanced effect of mutant granulocyte-colony-stimulating factor (KW-2228) on the growth of normal and leukemic hemopoietic progenitor cells in comparison with recombinant human granulocyte-colony-stimulating factor (G-CSF).

We tested the in vitro effect of a novel granulocyte colony-stimulating factor (G-CSF) derivative (KW-2228) on the growth of G-CSF-dependent hemopoietic progenitor cells: granulocyte precursor cells (CFU-G), leukemic blast progenitors freshly obtained from 9 patients with acute myeloblastic leukemia (AML) and cells of a G-CSF-dependent human AML cell line (OCI/AML 1a). KW-2228 showed a higher stimulating effect than recombinant human G-CSF (rhCSF) on CFU-G; 3 out of 9 leukemic blast progenitors and OCI/AML 1a cells. The difference in biochemical stability between rhG-CSF and KW-2228 was considered to explain the superior colony-stimulating activity of KW-2228. The results show that KW-2228 will be a new granulopoietic factor.

Amino Acid Sequence↗

Virus susceptibility of mouse hemopoietic cells in vitro: inhibition of granulocyte-macrophage precursor cells by Newcastle disease virus.

Normal mouse bone marrow cells were exposed to encephalomyocarditis virus (EMC), reovirus type 3 (REO3), influenza virus (FLU), and Newcastle disease virus (NDV) then assayed for granulocyte-macrophage precursor cells by the technique of colony formation in agar. Exposure to EMC, REO3, and FLU caused a slight but variable loss of colony-forming potential, whereas exposure to NDV caused a very marked loss. NDV acted directly on the cells, not indirectly through release of colony-inhibiting factors or destruction of colony-stimulating factor. Experiments with NDV inactivated by heat, ether, or ultraviolet irradiation indicated that colony inhibition was associated with fully infective virus, even though some of the inactivated preparations had retained full hemagglutinin, neuraminidase, or hemolytic activity.

Animals↗

[Radiosensitivity of clonogenic granulocytic macrophage cell precursors in the bone marrow and spleen of tumor-bearing mice].

Clonogenic granulocytic macrophagal cells-precursors (CFU-DC) of bone marrow and spleen of intact C57Bl/6 mice and those inoculated subcutaneously with LLC tumor cells do not substantially differ in their radiosensitivity; the concentration of CFU-DC in the spleen markedly varies as tumor grows. The values of Do and extrapolation number n for CFU-DC of the bone marrow are 0.9-1.4 and 1.5-3.0 Gy, and of the spleen, 0.8-1.6 and 1.0-2.6 Gy, respectively.

Animals↗

In vivo effects of interleukin-17 on haematopoietic cells and cytokine release in normal mice.

In order to gain more insight into mechanisms operating on the haematopoietic activity of the T-cell-derived cytokine, interleukin-17 (IL-17) and target cells that first respond to its action in vivo, the influence of a single intravenous injection of recombinant mouse IL-17 on bone marrow progenitors, further morphologically recognizable cells and peripheral blood cells was assessed in normal mice up to 72 h after treatment. Simultaneously, the release of IL-6, IL-10, IGF-I, IFN-gamma and NO by bone marrow cells was determined. Results showed that, in bone marrow, IL-17 did not affect granulocyte-macrophage (CFU-GM) progenitors, but induced a persistant increase in the number of morphologically recognizable proliferative granulocytes (PG) up to 48 h after treatment. The number of immature erythroid (BFU-E) progenitors was increased at 48 h, while the number of mature erythroid (CFU-E) progenitors was decreased up to 48 h. In peripheral blood, white blood cells were increased 6 h after treatment, mainly because of the increase in the number of lymphocytes. IL-17 also increased IL-6 release and NO production 6 h after administration. Additional in vitro assessment on bone marrow highly enriched Lin- progenitor cells, demonstrated a slightly enhancing effect of IL-17 on CFU-GM and no influence on BFU-E, suggesting the importance of bone marrow accessory cells and secondary induced cytokines for IL-17 mediated effects on progenitor cells. Taken together, these results demonstrate that in vivo IL-17 affects both granulocytic and erythroid lineages, with more mature haematopoietic progenitors responding first to its action. The opposite effects exerted on PG and CFU-E found at the same time indicate that IL-17, as a component of a regulatory network, is able to intervene in mechanisms that shift haematopoiesis from the erythroid to the granulocytic lineage.

Animals↗

Diffusion chamber hematopoiesis in marrow and spleen cells from mice infected with Rauscher leukemia virus (RLV-A).

Preleukemic and terminal phase marrow cells from RLV-A-infected mice placed within diffusion chambers and implanted into normal mice, maintained elevated levels of both erythroid and myeloid precursor cells, whereas normal control marrow cells grown within diffusion chambers in normal hosts did not. Splenic tissue from preleukemic and terminal mice when placed as a cellular suspension into diffusion chambers and implanted into normal recipients also maintained high erythroblast numbers. However, while some transient growth of myeloid precursor elements occurred in preleukemic spleen cultures, terminal spleen cultures displayed essentially no granulocytic precursor cell growth. In control spleen cultures, erythropoiesis and granulocytic precursor cell numbers were reduced to nondetectable levels after 4 days of culture.

Animals↗

Inhibition of granulocytic-macrophagic precursor cells (CFU-C) by heat-labile enterotoxin (LT) produced by Escherichia coli.

Enterotoxigenic strains of Escherichia coli cause diarrhea by production of heat-labile enterotoxin (LT) which acts through stimulation of membrane-bound adenylate-cyclase in epithelial cells. We studied in vitro production of LT by growing E. coli H 10407 in different synthetic media in comparison with Penassay broth. Non-toxigenic E. coli K12 was used as control. We obtained positive response in Y-1 cell assay for LT activity with all filtrates from E. coli H 10407 cultures. These filtrates inhibit 3H-thymidine uptake by Ehrlich Ascites Carcinoma (EAC) cells and the proliferation of granulocytic-macrophagic precursors (CFU-C) in murine bone marrow. Filtrates did not stimulate CFU-C in absence of CSF. Heat-treated (121 degrees C for 30 minutes) and dialyzed (molecular cut 15,000 daltons) filtrates lost their cytotoxicity against Y-1 cells maintaining the inhibitory activity on CFU-C proliferation. This phenomenon may be regarded as the result of a competitive mechanism between LT and CSF (Colony Stimulating Factor) on the receptor system of committed stem cells.

Animals↗

[Granulocyte-macrophage precursor cells in umbilical cord blood].

Authors study growth patterns of granulocytic-macrophagic progenitors in umbilical cord blood of 21 full-term newborns, using collagen gel culture method. Predominantly they obtain pure macrophagic colonies or mixed granulocytic colonies. After 7 days of incubation mean and SD of clusters in 103.22 +/- 75.88, and mean and SD of colonies is 34.26 +/- 23.1. After 14 days clusters falls down until 47.2 +/- 30.48, but colonies goes up to 74.2 +/- 32.78. Lineal regression analysis shows a correlation coefficient of 0.809 between 7 days and 14 days colonies. These results demonstrate the different behaviour between myelopoietic progenitor from umbilical cord blood and same progenitor from adult blood and are probably related to different nature of both progenitors.

Colony-Forming Units Assay↗

Granulocyte-macrophage precursor cell and colony-stimulating factor responses of mice infected with Salmonella typhimurium.

The response of granulocyte-macrophage progenitor cells (in vitro colony-forming cells) and of colony-stimulating (CS) factor in serum were studied in mice infected intraperitoneally with 10(3) viable Salmonella typhimurium. Increases in the number of colony-forming cells in marrow and spleen and increases in the serum level of CS factor occurred during the infection. There was no evidence to suggest that progressive infection was associated with failure of macrophage production. Medium rich in CS factor increased the bactericidal activity of macrophages in vitro and it was suggested that CS factor could be involved in macrophage activation.

Animals↗

Comparative effects of chlorozotocin and BCNU on hematopoietic precursor cells.

Comparative studies to determine the suppressive effects of chlorozotocin (2-[3-(2-chloroethyl)-3-nitrosoureido]-D-glucopyranose) and BCNU (1,3-bis[2-chloroethyl]-1-nitrosourea) on mouse and human hematopoietic precursor cells: granulocyte-macrophage precursor cells (CFU-gm), late erythroid precursor cells (CFU-e), and early erythroid precursor cells (BFU-e) were performed after in vitro incubation of 1 h with drug concentrations based on clinical administration levels. The suppressive effect of chlorozotocin on CFU-gm, BFU-e, and CFU-e hematopoietic precursor cells in the mouse was less than that of BCNU with the most significant difference seen in CFU-e colony formation. For human hematopoietic progenitor cells, however, the suppressive effect of chlorozotocin was far less than that of BCNU. When the effects of 40 micrograms/ml of chlorozotocin and 20 micrograms/ml of BCNU on human marrow were compared, there were statistically significant differences found for CFU-gm colony formation, and BFU-e and CFU-e colony numbers were significantly different for the two drugs at all comparable concentrations tested. Our results confirm the clinical data, and establish that the effects of chlorozotocin on human hematopoietic precursor cells are minimal.

Animals↗

Antigenic analysis of hematopoiesis. I. Expression of the My-1 granulocyte surface antigen on human marrow cells and leukemic cell lines.

Five monoclonal antibodies that identify the My-1 human granulocyte surface antigen were not reactive with other peripheral blood cells. These antibodies effected complement-dependent cytolysis of a large fraction of normal human marrow leukocytes. This My-1-positive marrow cell population consisted of morphologically identifiable granulocytic precursor cells. Colony-forming cells of the granulocyte-monocyte lineage (CFC-GM) did not express My-1, suggesting that the My-1 antigen is expressed later in normal granulocytic maturation. However, these antibodies did react with myeloid leukemic cell lines. The significance and potential utility of these probes for the understanding of granulopoietic differentiation is discussed.

Animals↗

Colony-forming ability of marrow from patients receiving immunotherapy during chemotherapy-induced remission in acute myeloid leukaemia.

An in vivo culture system, the agar diffusion chamber technique, has been used to measure the population of colony-forming precursor cells in the bone marrow of patients receiving immunotherapy during acute myeloid leukaemia in remission. The results of these assays indicate that (1) the level of committed granulocytic stem cells usually remains below the range found in normal marrow throughout remission, and (2) the maintenance of adequate cell counts in the blood may be due to increased cell production by these early granulocytic precursor cells. The relevance of these findings to the possible protective effect of immunotherapy against cytotoxic chemotherapy is discussed.

Adolescent↗