1.Chemopotentiation of Fresh Acute Myelogenous Leukemic Cells by Recombinant Human Granulocyte - Macrophage Colony - Stimulating Factor ( GM-CSF ) and Methotrexate.
Heung Tae KIM ; Jin Seok AHN ; Eun Shil KIM ; Yung Jue BANG ; Byoung Kook KIM ; Noe Kyeong KIM
Journal of the Korean Cancer Association 1998;30(2):357-369
No abstract available.
Granulocyte-Macrophage Colony-Stimulating Factor*
;
Granulocytes*
;
Humans*
;
Macrophages*
;
Methotrexate*
2.Plasma G-CSF and GM-CSF Concentrations and Expression of their Receptors on the Granulocyte in Children with Leukocytosis.
Won Seok CHOI ; Kyung Hwan RYU ; You Jeong KIM ; So Young KIM ; Hyun Hee KIM ; Wonbae LEE
Journal of the Korean Pediatric Society 2003;46(3):271-276
PURPOSE: Granulocyte-colony stimulating factor(G-CSF) and granulocyte macrophage-colony stimulating factor(GM-CSF) are principal cytokines in granulopoiesis and their physiologic effects are mediated through binding to specific cell surface receptors. Although it is known that the level of serum G-CSF and GM-CSF, and presentation of the receptors are increased in infectious diseases, there have been no studies to find the correlation between the granulopoiesis and leukocytosis. This study was designed to measure G-CSF and GM-CSF in leukocytosis and in control and to demonstrate the possible pathogenesis of granulopoiesis in leukocytosis using quantitative analysis of G- CSF, GM-CSF and their CSFr. METHODS: The plasma levels of G-CSF, GM-CSF of 13 children without leukocytosis and 14 children with leukocytosis were measured. Counts of cell surface G-CSFr and GM-CSFr were measured by combining anti G-CSFr and anti GM-CSFr monoclonal antibodies to their respective receptors by using quantitative flow cytometric assay. RESULTS: There was no significant difference betweeen the plasma concentration of G-CSF and GM-CSF in acute leukocytosis and in the control group. However, levels of G-CSFr in acute leukocytosis decreased significantly compared to the control(P=0.012) and the levels of GM-CSFr in both groups revealed no significant difference. CONCLUSION: Increase in the number of leukocyte in leukocytosis was mediated by increasing the number of neutrophil, and increased plasma concentration of G-CSF may be the cause of neutrophilia. But GM-CSF did not have any influence on leukocytosis.
Antibodies, Monoclonal
;
Child*
;
Communicable Diseases
;
Cytokines
;
Granulocyte Colony-Stimulating Factor*
;
Granulocyte-Macrophage Colony-Stimulating Factor*
;
Granulocytes*
;
Humans
;
Leukocytes
;
Leukocytosis*
;
Neutrophils
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Plasma*
;
Receptors, Cell Surface
;
Receptors, Granulocyte Colony-Stimulating Factor
;
Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
3.Plasma G-CSF and GM-CSF Concentration and Amount of Their Receptors on the Granulocyte in Kawasaki Disease.
Young Kyoung YOO ; Gibum LEE ; Hyun Hee KIM ; Soo Young KIM ; You Jeong KIM ; Wonbae LEE
Journal of the Korean Pediatric Society 2003;46(4):376-381
PURPOSE: This study aimed to demonstrate the possible pathogenesis of granulopoiesis in patients of Kawasaki disease(KD) using quantitative analysis of G-CSF, GM-CSF and their CSFr. METHODS: The plasma levels of G-CSF, GM-CSF, G-CSFr and GM-CSFr were studied in 14 patients in the acute phase of KD; 13 children with normal peripheral white blood cell counts were used as the normal control group. The plasma concentration of G-CSF, GM-CSF were analyzed by ELISA. The G-CSFr and GM-CSFr on the peripheral granulocytes were analyzed by a quantitative flow cytometric assay and QuantiBRITE, and the quantitative changes of receptors which did not combine with G-CSF and GM-CSF were measured. RESULTS: The total number of leukocytes in KD was similar to normal control group, but the leukocytes increased according to the number of neutrophils. The plasma concentration of G-CSF were decreased similar to normal control group(P=0.133), but that of GM-CSF decreased more than the normal control group(P=0.227). The quantity of G-CSFr, GM-CSFr were revealed to be no less than the normal control(P=0.721, P=0.912). After incubation with excessive G-CSF, the expressed G-CSFr on the neutrophils were decreased in both groups(P=0.554). The quantities of expressions of GM- CSFr on the neutrophil after incubation with the excessive GM-CSF were always increased in both groups(P=0.255). The amount of GM-CSFr of neutrophils are in proportion to total white blood cells (r=0.788, P=0.035), but it wasn't in the case of KD(P=0.644). CONCLUSION: The leukocytosis in KD that mediated by increasing neutrophil was not correlated with the plasma concentrations of G-CSF and GM-CSF, and the amount of expression of G-CSFr and GM-CSFr on granulocyte. It is possible that the reduction of concentration of GM-CSF results by increasing the active GM-CSFr.
Child
;
Enzyme-Linked Immunosorbent Assay
;
Granulocyte Colony-Stimulating Factor*
;
Granulocyte-Macrophage Colony-Stimulating Factor*
;
Granulocytes*
;
Humans
;
Leukocyte Count
;
Leukocytes
;
Leukocytosis
;
Mucocutaneous Lymph Node Syndrome*
;
Neutrophils
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Plasma*
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Receptors, Granulocyte Colony-Stimulating Factor
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Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
4.Hematopoietic Recovery of Peripheral Blood Stem Cells Stored at 4degrees C.
Seok Goo CHO ; Eun Jee OH ; Jun Mo LEE ; Hoon Kyo KIM ; Kyung Shick LEE ; Chun Choo KIM
Journal of the Korean Cancer Association 2000;32(3):647-654
PURPOSE: Cryopreservation has been the standard method of storing hematopoietic cells for the past 20 years, but this prdegrees Cedure is laborious and expensive. So, we evaluated the hematopoietic recovery of stored PBSCs at 4degrees C for a variable storage period MATERIALS AND METHODS: Eight leukapheresis products were kept unprdegrees Cessed at 4degrees C for 96 hours. To evaluate the effect of storage period on the hematopoietic recovery of PBSCs, assays for viability of mononuclear cells (MNCs), CFU-GM colony counts and CD34 cell counts were performed every 24 hours after PBSC collection. We tried to compare hematopoetic recovery of stored PBSCs at 4degrees C with that of cryopreserved PBSCs by using repeated measures ANOVA. RESULTS: Viability of MNCs, CFU-GM colony counts and CD34 cell counts were monitored at 24 hour, 48 hour, 72 hour and 96 hour after PBSC collection. Data are expressed as percentage of baseline value and shown as mean s.d.; MNCs viability (96+/-2%, 94+/-2%, 92+/-2%, 88+/- 3%), CFU-GM colony counts (87+/-10%, 79+/-11%, 65+/-13%, 56+/-15%), and CD34 cell counts (93+/-13%, 93+/-12%, 88+/-14%, 85+/-19%). After storing PBSCs at 4degrees C for 96 hours, viability of MNCs and CFU-GM colony counts were significantly reduced (p<0.05) except CD34 cell concentration (p>0.05). Prdegrees Cedures of controlled-rate freezing and thawing resulted in a notable loss of viability (77+/-9%) and CFU-GM colony count (71+/-29%). CFU-GM colony counts of 72 hour-stored PBSCs at 4degrees C was similar to those of cryopreserved PBSCs. CONCLUSION: If G-CSF mobilized PBSCs are stored at 4degrees C in less than 72 hours after collection, those hematopoietic recovery would be comparable to that of cryopreserved stem cells which are achieved by the rate-control freezer.
Bezafibrate
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Cell Count
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Cryopreservation
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Freezing
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Granulocyte Colony-Stimulating Factor
;
Granulocyte-Macrophage Progenitor Cells
;
Leukapheresis
;
Stem Cells*
5.The Effect of Granulocyte Colony Stimulating Factor and Granulocyte Macrophage Colony Stimulating Factor on the Preimplantation Development and Implantation in Mouse Embryos.
Chung Hoon KIM ; Eun Ju PARK ; Jong Yoon HWANG ; Seok Ho HONG ; Sung Hoon KIM ; Hee Dong CHAE ; Byung Moon KANG
Korean Journal of Obstetrics and Gynecology 2002;45(1):126-132
OBJECTIVE: To investigate the influence of granulocyte colony stimulating factor (G-CSF) and granulocyte macrophage colony stimulating factor (GM-CSF) on preimplantation development and implantation in mouse embryos. MATERIAL AND METHODS: Eight-cell stage mouse embryos were cultured for 96 hours with G-CSF or GM-CSF at concentrations of 10 pg/ml, 100 pg/ml, 1 ng/ml and 10 ng/ml. Embryos not treated with G-CSF or GM-CSF were served as control. The percentages of embryos which developed to expanded, hatched blastocyst stage and in vitro implantation at 96 hours were determined. Results were analyzed with Kolmogorov-Smirnov test and analysis of variance (ANOVA). The statistical significance was defined as p<0.05. RESULTS: The percentages of fully expanded blastocysts in all G-CSF and GM-CSF treatment groups were not significantly different from the control. The percentages of hatched blastocysts were significantly higher in 100 pg/ml and 10 ng/ml of G-CSF treatment group compared to the control (p<0.05, p<0.05, respectively). The percentages of hatched blastocysts were significantly lower in 1 ng/ml of GM-CSF treatment group compared to the control, 10 pg/ml, and 100 pg/ml of GM-CSF treatment group (p<0.05, p<0.05, p<0.05, respectively), and the percentages of hatched blastocysts were also significantly lower in 10 ng/ml of GM-CSF treatment group compared to the control and 100 pg/ml of GM-CSF treatment group (p<0.05, p<0.05, respectively). The percentages of implanted blastocysts in vitro were significantly higher following incubation with all concentrations of G-CSF compared to the control and, especially in 100 pg/ml and 10 ng/ml of G-CSF treatment groups compared to the control and other treatment groups. The percentages of implanted blastocysts in vitro were significantly higher in 10 pg/ml of GM-CSF treatment group than the control and 100 pg/ml of GM-CSF treatment groups (p<0.05, p<0.05, respectively). CONCLUSION: G-CSF and GM-CSF might influence on embryonic development and implantation in mouse embryos.
Animals
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Blastocyst
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Colony-Stimulating Factors*
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Embryonic Development
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Embryonic Structures*
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Female
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Granulocyte Colony-Stimulating Factor
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Granulocyte-Macrophage Colony-Stimulating Factor*
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Granulocytes*
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Mice*
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Pregnancy
6.Serum amyloid A inhibits dendritic cell differentiation by suppressing GM-CSF receptor expression and signaling.
Ji Cheol KIM ; Young Su JUNG ; Ha Young LEE ; Joon Seong PARK ; Yoe Sik BAE
Experimental & Molecular Medicine 2017;49(8):e369-
In this study, we report that an acute phase reactant, serum amyloid A (SAA), strongly inhibits dendritic cell differentiation induced by GM-CSF plus IL-4. SAA markedly decreased the expression of MHCII and CD11c. Moreover, SAA decreased cell surface GM-CSF receptor expression. SAA also decreased the expression of PU.1 and C/EBPα, which play roles in the expression of GM-CSF receptor. This inhibitory response by SAA is partly mediated by the well-known SAA receptors, Toll-like receptor 2 and formyl peptide receptor 2. Taken together, we suggest a novel insight into the inhibitory role of SAA in dendritic cell differentiation.
Dendritic Cells*
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Granulocyte-Macrophage Colony-Stimulating Factor*
;
Interleukin-4
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Receptors, Formyl Peptide
;
Receptors, Granulocyte-Macrophage Colony-Stimulating Factor*
;
Serum Amyloid A Protein*
;
Toll-Like Receptors
7.Application of Apoptogenic Pretreatment to Enhance Anti-tumor Immunity of Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF)-secreting CT26 Tumor Cells.
Do Youn JUN ; Elizabeth M JAFFEE ; Young Ho KIM
Immune Network 2005;5(2):110-116
BACKGROUND: As an attempt to develop a strategy to improve the protective immune response to GM-CSF-secreting CT26 (GM-CSF/CT26) tumor vaccine, we have investigated whether the apoptogenic treatment of GM-CSF/CT26 prior to vaccination enhances the induction of anti-tumor immune response in mouse model. METHODS: A carcinogen- induced mouse colorectal tumor, CT26 was transfected with GM-CSF gene using a retroviral vector to generate GM-CSF-secreting CT26 (CT26/GM-CSF). The CT26/GM-CSF was treated with gamma-irradiation or mitomycin C to induce apoptosis and vaccinated into BALB/c mice. After 7 days, the mice were injected with a lethal dose of challenge live CT26 cells to examine the protective effect of tumor vaccination in vivo. RESULTS: Although both apoptotic and necrotic CT26/GM-CSF vaccines were able to enhance anti-tumor immune response, apoptotic CT26/GM-CSF induced by pretreatment with gamma-irradiation (50,000 rads) was the most potent in generating the anti-tumor immunity, and thus 100% of mice vaccinated with the apoptotic cells remained tumor free for more than 60 days after tumor challenge. CONCLUSION: Apoptogenic pretreatment of GM-CSF-secreting CT26 tumor vaccine by gamma-irradiation (50,000 rads) resulted in a significant enhancement in inducing the protective anti-tumor immunity. A rapid induction of apoptosis of CT26/GM-CSF tumor vaccine at the vaccine site might be critical for the enhancement in anti-tumor immune response to tumor vaccine.
Animals
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Apoptosis
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Colony-Stimulating Factors*
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Colorectal Neoplasms
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Granulocyte-Macrophage Colony-Stimulating Factor
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Mice
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Mitomycin
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Vaccination
;
Vaccines
;
Zidovudine
8.Effect of GM-CSF to the M-VAC Chemotherapy Induced Leukopenia in Patients with Urothelial Cancer.
Jong Bo CHOI ; Dong Sun KIM ; Jae Heung CHO
Korean Journal of Urology 1994;35(2):151-155
Granulocyte macrophage-colony stimulating factor (GM-CSF) occupies a central position in the regulation of hematopoietic responses. GM-CSF not only signals proliferations of granulocyte-macrophage but also drives these cells into differentiation and activates mature cells of the GM-CSF sensitive lineage. Myelosuppression that is induced by M-VAC (methotrexate, vinblastine, doxorubicin, cisplatinum) chemotherapy brings many problems in successful treatment such as sepsis, dose reduction, delaying the schedule. Granulocyte-macrophage colony stimulating factor is introduced hopefully as a new solution for these problems. So we evaluated the efficacy and safety of GM-CSF in leukopenia induced by M-VAC chemotherapy in patients with urothelial cancer. GM-CSF was administered at 200ug subcutaneously in 10 M-VAC cycles of 6 patients on 5th and 6th day after M-VAC therapy. Sixteen cycles, by which only M-VAC chemotherapy was administered without GM-CSF. of the other 6 patients served as control group. Mean white blood cell count in peripheral blood at M-VAC 2nd day and 15th day was 5,630/mm3 and 4,240/mm3 in GM-CSF administered cycles, 6,58l/mm3and 3,613/mm3 in non GM-CSF administered cycles. There was no delayed cycle in administration of MTX and vinblastine at M-VAC 15th day in the cycles with GM-CSF. There was no significant side effects caused by GM- CSF. The result indicates that GM-CSF can be used safely and effectively against leukopenia after M-VAC chemotherapy of urothelial cancer.
Appointments and Schedules
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Colony-Stimulating Factors
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Doxorubicin
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Drug Therapy*
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Granulocyte-Macrophage Colony-Stimulating Factor*
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Granulocytes
;
Humans
;
Leukocyte Count
;
Leukopenia*
;
Sepsis
;
Vinblastine
9.A Case of Pulmonary Alveolar Proteinosis with Spontaneous Resolution.
Seung Bum NAM ; Kwang Young PARK ; Ho Jin LEE ; Jae Wook JUNG ; Yoon Hee CHOI ; Hyo Seok KIM ; Cheol Hyeon KIM ; Jae Cheol LEE
Tuberculosis and Respiratory Diseases 2007;63(3):294-298
Pulmonary alveolar proteinosis is a rare disorder that is characterized by the abundant accumulation of surfactant-derived material within the alveolar spaces and distal bronchioles. Although the findings of homogenous ground-glass opacities overlaid by thickened septa, which form a "crazy paving" pattern on high-resolution computed tomography, can assist in making a diagnosis, a lung biopsy is usually required. This disorder has a variable clinical course, from spontaneous resolution to respiratory failure and death. While a whole lung lavage has been the standard treatment since the early 1960s, GM-CSF therapy has been attempted based on the recently suggested pathogenetic mechanism. We report a case of pulmonary alveolar proteinosis that resolved spontaneously after an open lung biopsy.
Biopsy
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Bronchioles
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Bronchoalveolar Lavage
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Diagnosis
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Granulocyte-Macrophage Colony-Stimulating Factor
;
Lung
;
Pulmonary Alveolar Proteinosis*
;
Respiratory Insufficiency
10.Effect of combination gene therapy with herpes simplex virus thymidine kinase suicidal gene and granulocyte-macrophage colony-stimulating factor gene in murine melanoma model.
Korean Journal of Medicine 1999;57(4):397-401
No abstract available.
Genetic Therapy*
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Granulocyte-Macrophage Colony-Stimulating Factor*
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Herpes Simplex*
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Melanoma*
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Phosphotransferases*
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Simplexvirus*