Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00035 (CSF)
 30,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The susceptibility of mouse bone marrow colony forming cells (CFUc) to three different types of proliferation inhibitors in capillary semisolid agar gel was studied. GI-3, a target specific peptide containing granulocyte fraction, T4-1, an oligospecific thymic factor of proteid nature, and the alkylating cytostatics dianhydrogalactitol (DAD) inhibit myeloid colony formation as a function of concentration. The respective MED values amount to 8, 10, and 0.002 microgram/ml. When compared with this same parameter 3H-TdR incorporation into DNA of liquid bone marrow cultures showed a single fold charge for the endogenous inhibitors (GI-3, T4-1) for the cytostatic (DAD) a 3 to 4 fold lower difference. It was demonstrated, that in competitive antagonism of GI-3 and colony stimulating factor the inhibitor prevails over CSF.
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PMID:Control of CFUc proliferation by selective endogenous inhibitors. 4 9

Because Corynebacterium parvum has tumor-inhibitory properties and stimulates granulocyte-macrophage production, it may have clinical value in combination with chemotherapy. The leukopoietic effect of killed suspensions of C. parvum was studied in mice using the technique of in vitro clonal culture of hematopoietic cells. After C. parvum injection, there was a prompt, sustained elevation of serum colony-stimulating factor followed by an increase in granulocyte-macrophage precursor cells in the spleen and increases in blood mononuclear and granulocyte cells. Colony-stimulating factor production is suggested as a major mechanism of stimulation of granulocyte-macrophage proliferation by C. parvum. Since rapidly proliferating hematopoietic cells may have increased sensititity to cytotoxic agents, the details of hematopoietic stimulation by C. parvum may be critical in the sequential timing of combined C. parvum and chemotherapy treatment to obtain maximal tumor inhibition and minimal hematopoietic toxicity.
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PMID:Effect of Corynebacterium parvum on colony-stimulating factor and granulocyte-macrophage colony formation. 30 Jun 51

Eighteen surgical patients were studied to determine the effect of anesthesia (general or spinal) and surgery on serum and urinary colony-stimulating factor(s) (CSF). CSF is a leukopoietin that stimulates proliferation of macrophages and granulocytes from bone marrow precursor cells. CSF was assayed by adding aliquots of serum or urine to semisolid agar cultures of bone marrow cells and scoring the number of colonies developing after 7 days of incubation. In all but 1 case, a 3- to 30-fold increase in the 24 hour excretion of urinary CSF was seen on the day of surgery and the first postoperative day. CSF urinary excretion began declining toward normal by the second postoperative day. A parallel increase in granulocyte count, a delayed rise in monocytes, and a decline in absolute lymphocyte counts were also observed. The data suggest that immediately postoperatively there may be a strong stimulus to granulocyte/macrophage proliferation. More rapidly proliferating cells would be anticipated to have increased vulnerability to toxicity from cell cycle-active chemotherapeutic agents.
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PMID:Effect of surgery on granulocyte/macrophage colony-stimulating factor. 30 79

At the earliest stages of fetal hepatic hemopoiesis in CBA mice (11-12 days gestation), colony stimulating activity could be found only in peripheral blood, yolk-sac fluid and media conditioned by yolk-sacs (YSCM). The colony stimulating factor (GM-CSF) from YSCM was able to be concentrated by absorption to DEAE-cellulose and subsequent elution. Titration of this material produced a sigmoid dose-response curve in agar cultures of adult CBA bone marrow cells. Unlike the high proportion of granulocyte colonies stimulated by the GM-CSF from mouse lung conditioned medium, all concentrations of YSCM produced a high proportion of macrophage colonies after 7 days of incubation. Mixing experiments eliminated the possibility that a specific inhibitor preventing granulocyte differentiation was present in YSCM. Fetal liver cells were relatively unresponsive to YSCM, but their ability to respond increased with gestational age. When stimulated by YSCM, fetal liver colony forming cells from mice of all gestational ages produced more than 90% macrophage colonies after 7 days of incubation. The experimental data suggest that the proliferation and differentiation of granulocyte and macrophage precursors in the early fetal liver could be controlled by a fetal type of GM-CSF favoring macrophage production.
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PMID:Sources and nature of granulocyte-macrophage colony stimulating factor in fetal mice. 30 47

The effects of intraperitoneal Ehrlich ascites tumor (ET) growth on the kinetics of hemopoietic stem cells in the host bone marrow were studied using the spleen colony and the soft agar culture techniques. There is a decrease in spleen colony forming capacity of bone marrow of ET bearing mice, whereas in vitro assays of the committed macrophage granulocyte precursors, by the soft agar method, show that in the same circumstances a high yield of granulopoietic colonies can still be obtained. A shift of the CFU-c/CFU-s ratio from 15 to 36 thus occurs. Moreover, ascitic fluid from tumoral mice displays strong activity as CSF on normal mouse marrow, twice as strong as the standard mouse embryo CSF. When conditioned medium from cultures of ET cells (ET-CM) is tested, the pattern of agar colonies obtained is different from the previously obtained pattern of growth kinetics; furthermore many colonies are composed of undifferentiated cells. The hypothesis is suggested that among the variety of known CSF's, the ET-CM represents a unique factor, capable of inducing proliferation of marrow CFU-c, but only limited differentiation.
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PMID:Different colony stimulating activity by tumoral ascitic fluid and conditioned media. 30 30

Differentiation and proliferation of almost all hemopoietic cell lines can now be studied in vitro. Cloning techniques and suspension cultures allow the study of proliferation of the multipotential hemopoietic progenitor cell and the committed progenitors for granulocytes, macrophages, eosinophils, megakaryocytes, and erythrocytes. The proliferation of each of the committed progenitor cells is controlled by specific glycoproteins and two of these have recently been purified: granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin. The rate of proliferation of the GM-progenitor cells and their pattern of differentiation depends on the concentration of the hormone. At low concentrations of GM-CSF (10(-11) M) fewer progenitor cells are stimulated and macrophage colonies rather than granulocyte colonies develop. The change in the direction of granulocyte-macrophage differentiation appears to be related to a) the concentration of GM- CSF and b) the different sensitivity of a subpopulation of monocyte colony-forming cells which are responsive to GM-CSF even at low concentrations of the regulator. Analysis of the rate of RNA synthesis by bone marrow cells has shown that GM-CSF stimulates the mature nondividing end cells of differentiation (ie, polymorphs) as well as the progenitor cells. Although GM-CSF and erythropoietin have been radiolabeled, binding studies have been hampered by the loss of biologic activity during the labeling procedure and the heterogeneity of the target cells to which the regulators bind. Surface proteins and receptors for erythrocytes have been well characterized but the relationships between these proteins and the cell surface proteins of nucleated blood cells is not well understood. It appears that some proteins are lost from the cell surface during the development of granulocytes, which are retained on the surface of the B lymphocyte. Other proteins such as chemotactic receptors and complement receptors only appear on the mature cells. External radiolabeling of the granulocyte surface using iodogen yielded a simple profile of 125I-labeled proteins when analyzed by sodium dodecyl sulphate polyacrylamide gel electrophoresis.
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PMID:Regulation of hemopoietic cell differentiation and proliferation. 30 73

The heterogeneity among progenitor cells of granulocytes and macrophages capable of forming colonies in vitro (CFU-c) is analysed. If specific culture conditions and stimuli are used, it is possible to discriminate among three subpopulations of CFU-c. CFU-c directly responding to CSF prepared from pregnant mouse uteri are characterized by a density of 1.075 g.cm-3. The G1-phase cells of this CFU-c subpopulation have a sedimentation rate of 4.8 mm.h-1. CFU-c of two additional subpopulations are induced to proliferate by enhancing factors present in serum of mice injected with endotoxin 18 hours earlier and in lysate of rat erythrocytes. CFU-c responding to postendotoxin serum have a density of 1.070 g.cm-3 and a sedimentation rate of 4.3 mm.h-1 (G1 cells). The CFU-c responding to erythrocyte lysate have a density of 1.080 g.cm-3 and a sedimentation rate of 5.3 mm.h-1 (G1 cells). The calculated diameters of G1-phase cells of these three CFU-c subpopulations range from 7.4 to 7.6 micron and are not significantly different. It is proposed that the three CFU-c detected represent three sequential maturation stages of granulocyte/macrophage progenitor cells. These cells are similar in size but increase in density (1.070 g.cm-3 to 1.080 g.cm-3) as they mature.
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PMID:The physical separation of three subpopulations of granulocyte/macrophage progenitor cells from mouse bone marrow. 31 50

This study was undertaken to determine whether adrenal corticosteroids suppress meningeal inflammation in experimental pneumococcal meningitis in rabbits and, if so, whether the mechanism of suppression involves inhibition of chemotactic activity in CSF or modification of granulocyte responses to inflammation mediators. It was found that methyl prednisolone, administered intramuscularly in doses of 15 or 30 mg/kg 24 hr and 48 hr after induction of meningitis, significantly reduced (p less than 0.01) the mass of granulocytes present in the meninges 72 hr after infection, the time of maximum meningeal inflammation. The larger dose of steroid produced approximately twice the suppressive effect of the smaller dose (p less than 0.05). The regime of methyl prednisolone that produced maximal suppression of meningeal inflammation (30 mg/kg/day) did not alter CSF chemotactic activity or chemotactic responsiveness and phagocytic activities of granulocytes from rabbits with meningitis. However, steroid therapy inhibited an increase in granulocyte adherence that was observed in untreated animals with meningitis (p less than 0.05). Thus methyl prednisolone in doses of 15 and 30 mg/kg given daily to rabbits with pneumococcal meningitis produced a suppressive effect on meningeal inflammation that was dose-dependent and was possibly mediated by inhibition of granulocyte adherence.
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PMID:Experimental pneumococcal meningitis. IV. The effect of methyl prednisolone on meningeal inflammation. 65 62

CSF-dependent myeloid colony growth can be augmented or inhibited by a number of modulating factors. PGs of the E series are known to inhibit colony formation. The antagonistic actions of PGE and PGF in many biological systems prompted us to compare their effects on myelopoiesis in vitro. PGF2alpha at an optimal concentration of 1 x 10(-9)M increased colony formation by 50% over that stimulated by CSF alone. Similar augmentation was also observed from 16,16-dimethyl PGF2alpha, PGF1alpha, 6-keto PGF1alpha, and MIX. In contrast PGE1, PGE2, and 15(S),15-methyl PGE1 inhibited colony growth. Simulation by PGF reflected an absolute increase in granulocytic colonies, whereas inhibition by PGE affected both granulocyte and macrophage colony formation. The relative levels of PGE and PGF may play a determining role in the modulation of granulopoiesis.
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PMID:Modulation of granulopoiesis: opposing roles of prostaglandins F and E. 73 76

In a study of 60 head-injured patients inhibition of phagocytosis by neutrophil granulocytes was observed over a period of up to 5 weeks. This inhibition of phagocytosis could be correlated with the severity of head injury as well as with the state of unconsciousness at the time of the investigation. No correlation was found between neutrophil granulocyte counts and the inhibition of phagocytosis. A good correlation could be demonstrated between the level of lumbar CSF 5-HIAA and the inhibition of phagocytosis. After in vitro incubation with albumin the cells showed a recovery of phagocytosis. Electron micrographs of the cells showed ultrastructural appearances suggesting a changed permeability of the plasma membrane and, in addition, alterations in the cytoplasmic region beneath the plasma membrane. It is suggested that head injury may influence the pituitary-adrenal system and the autonomic nervous system, giving changes of neutrophil function and of neurotransmitter metabolism; these changes may represent an adaptation mechanism.
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PMID:Biochemical and ultrastructural aspects of the inhibited phagocytosis by neutrophil granulocytes in acute brain-damaged patients. 83 33


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