scholarly journals Highly Sensitive Enzyme-Linked Immunosorbent Assay for Marograstim (KW-2228), a Mutant of Human Granulocyte Colony-Stimulating Factor.

1992 ◽  
Vol 15 (3) ◽  
pp. 121-129 ◽  
Author(s):  
Takashi KUWABARA ◽  
Shuzo OKUMURA ◽  
Satoshi KOBAYASHI ◽  
Tadashi HIRATA
Keyword(s):  
Immunosorbent Assay ◽  
Enzyme Linked Immunosorbent Assay ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Highly Sensitive ◽  
Stimulating Factor

scholarly journals Granulocyte Colony-Stimulating Factor in Amniotic Fluid

1995 ◽  
Vol 3 (4) ◽  
pp. 140-144 ◽  
Author(s):  
B. Denise Raynor ◽  
Penny Clark ◽  
Patrick Duff
Keyword(s):  
Amniotic Fluid ◽  
Immunosorbent Assay ◽  
Intrauterine Infection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Csf Levels ◽  
The Mean ◽  
Stimulating Factor ◽  
Factor G

Objective: The purpose of this study was to determine if granulocyte colony-stimulating factor (G-CSF) is normally present in amniotic fluid and then to determine if amniotic-fluid G-CSF levels are affected by labor and intrauterine infection.Methods: Amniotic fluid was collected from 35 patients in 4 groups: no labor, early labor, late labor, and labor plus chorioamnionitis. G-CSF levels were measured by enzyme-linked immunosorbent assay (ELISA).Results: The mean amniotic-fluid G-CSF concentrations prior to labor were lower than during labor (0.49 ± 0.25 ng/ml for prior to labor vs. 1.83 ± 1.0 ng/ml for labor, P < 0.001). With chorioamnionitis, the mean levels were elevated compared with normal labor (25.0 ± 4.8 ng/ml for chorioamnionitis vs. 1.83 ± 1.0 ng/ml for normal labor, P < 0.0001). In early and late labor, G-CSF was higher than prior to labor (0.49 ± 0.25 ng/ml for no labor vs. 1.48 ± 1.0 ng/ml for early labor, P < 0.02, vs. 2.2 ± 0.8 ng/ml for late labor, P < 0.0005). The mean concentrations in early and late labor were not different.Conclusions: G-CSF is present in amniotic fluid and increased with labor. When labor is complicated by chorioamnionitis, G-CSF is significantly elevated.

scholarly journals Serum concentrations of granulocyte colony-stimulating factor in healthy term and preterm neonates and in those with various diseases including bacterial infections

Blood ◽  
1993 ◽  
Vol 82 (10) ◽  
pp. 3177-3182 ◽  
Author(s):  
P Gessler ◽  
N Kirchmann ◽  
R Kientsch-Engel ◽  
N Haas ◽  
P Lasch ◽  
...  
Keyword(s):  
Bacterial Infections ◽  
Assay Method ◽  
Preterm Neonates ◽  
Enzyme Linked Immunosorbent Assay ◽  
Granulocyte Colony Stimulating Factor ◽  
Serum Concentrations ◽  
Colony Stimulating Factor ◽  
Csf Levels ◽  
Stimulating Factor

Abstract The neonate is uniquely susceptible to severe and overwhelming bacterial infections. One of the most important deficits in the neonatal host defense system seems to be a quantitative and qualitative deficiency of the myeloid and the phagocytic system. Future optimal therapy of neonatal sepsis may include the use of adjuvant immunologic therapy. Granulocyte colony-stimulating factor (G-CSF) has been shown to induce neutrophilia and to enhance mature effector neutrophil function. To evaluate the role of G-CSF with respect to infection, we examined serum levels of G-CSF in term and preterm neonates, using an enzyme-linked immunosorbent assay method. G-CSF levels in healthy neonates showed peak levels up to 7 hours after birth, followed by an increase in total neutrophil cell (TNC) counts. Both G-CSF levels determined between 4 and 7 hours after birth and peak TNC counts correlated with the gestational age of the neonates. The state of nutrition, maternal treatment with glucocorticoids, maternal infection and hypertension, and the mode of delivery influenced peak G-CSF levels. Neonates with signs of infection between 4 and 7 hours after birth had higher levels of G-CSF than did healthy neonates (1,312 +/- 396 pg/mL v 176 +/- 19 pg/mL). In conclusion, the presented results of serum concentrations of G-CSF in relation to TNC counts and various diseases suggests an important role of G-CSF in the regulation of granulopoiesis during the neonatal period.

Human monocytes express functional receptors for granulocyte colony– stimulating factor that mediate suppression of monokines and interferon-γ

Blood ◽  
2000 ◽  
Vol 95 (1) ◽  
pp. 270-276 ◽  
Author(s):  
Eva-Maria Boneberg ◽  
Lars Hareng ◽  
Florian Gantner ◽  
Albrecht Wendel ◽  
Thomas Hartung
Keyword(s):  
Flow Cytometry ◽  
Whole Blood ◽  
Receptor Expression ◽  
Human Neutrophils ◽  
Enzyme Linked Immunosorbent Assay ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Ifn Γ ◽  
Stimulating Factor

In a double-blind, placebo-controlled, randomized study, 10 healthy men received either a single dose of 480 μg granulocyte colony-stimulating factor (G-CSF) or saline. Blood taken from the volunteers was stimulated with 10 μg/mL endotoxin and released cytokines were measured by enzyme-linked immunosorbent assay. Expression of G-CSF receptors on leukocytes was examined by flow cytometry and reverse transcriptase-polymerase chain reaction. Functional activity of these receptors was tested by challenging isolated leukocyte populations to release cytokines with endotoxin in the presence of G-CSF. The G-CSF treatment attenuated the release of the proinflammatory cytokines tumor necrosis factor (TNF)-, interleukin (IL)-12, IL-1β, and interferon (IFN)-γ in ex vivo lipopolysaccharide (LPS)-stimulated whole blood. In blood from untreated volunteers the presence of G-CSF in vitro also attenuated the LPS-stimulated release of these cytokines. G-CSF in vitro also attenuated TNF- release from elutriation-purified monocytes. In the presence of 10 ng/mL recombinant TNF-, the attenuation of LPS-inducible IFN-γ release by G-CSF was blunted in whole blood. However, G-CSF had no such effect on IFN-γ release from isolated lymphocytes stimulated with anti-CD3 or a combination of TNF- and IL-12. G-CSF receptor expression was detected in human neutrophils and monocytes but not in lymphocytes by means of RT-PCR as well as flow cytometry. These results indicate that G-CSF receptors expressed on monocytes are functional in modulating monokine release. We conclude that the attenuation of IFN-γ release from lymphocytes is not a direct effect of G-CSF on these cells but is rather due to the inhibition of monocytic IL-12 and TNF- release by G-CSF. (Blood. 2000;95:270-276)

scholarly journals Regulation of granulocyte colony-stimulating factor and granulocyte- macrophage colony-stimulating factor expression by oncostatin M

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 33-37 ◽  
Author(s):  
TJ Brown ◽  
J Liu ◽  
C Brashem-Stein ◽  
M Shoyab
Keyword(s):  
Protein Expression ◽  
Oncostatin M ◽  
Enzyme Linked Immunosorbent Assay ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Cellular Expression ◽  
Factor Expression ◽  
Culture Supernatants ◽  
Stimulating Factor

Oncostatin M (OM) is structurally and functionally related to a subclass of hematopoietic cytokines including leukemia-inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), granulocyte colony- stimulating factor (G-CSF), and interleukin-6 (IL-6). Using human endothelial cells (HEC) as a model for cytokine regulation of hematopoietic growth factor expression, we tested OM as an inducer of colony-stimulating activity. Colony-forming cell assays supplemented with culture supernatants from OM-treated HEC contained a threefold increase in colony-forming unit granulocyte-macrophage colonies. Specific immunoassay (enzyme-linked immunosorbent assay) of culture supernatants indicated that OM treatment of HEC resulted in a dose- and time-dependent increase in the accumulation of G-CSF and granulocyte- macrophage CSF (GM-CSF) (> 28-fold). The ED50 for OM induction of G-CSF and GM-CSF protein expression was 17 and 7 pmol/L, respectively. Increased protein expression was associated with a similar increase in steady-state expression of G-CSF and GM-CSF mRNA. Furthermore, a period of 12 to 24 hours elapsed before there were measurable increases in CSF expression, suggesting that OM may stimulate CSF production through a mechanism requiring the synthesis or activation of a secondary mediating factor or pathway. These findings provide the first evidence that OM may regulate myelopoiesis by inducing the cellular expression of hematopoietic growth factors.

scholarly journals Quantitation and identification of human monocytic colony-stimulating factor in human serum by enzyme-linked immunosorbent assay

Blood ◽  
1988 ◽  
Vol 72 (3) ◽  
pp. 886-892 ◽  
Author(s):  
T Hanamura ◽  
K Motoyoshi ◽  
K Yoshida ◽  
M Saito ◽  
Y Miura ◽  
...  
Keyword(s):  
Human Serum ◽  
Immunosorbent Assay ◽  
High Performance ◽  
Reversed Phase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Colony Stimulating Factor ◽  
Elisa System ◽  
Anticancer Chemotherapy ◽  
Average Serum ◽  
Stimulating Factor

Abstract An enzyme-linked immunosorbent assay (ELISA) system for the quantitation of human monocytic colony-stimulating factor (hM-CSF) was established, which was based on the “dual antibody immunometric sandwich” principle using horse and rabbit polyvalent antibodies against human urinary colony-stimulating factor (CSF-HU). The minimal detectable level of hM-CSF was 10 U/mL, and the assays showed good reproducibility. As measured by this method, the average serum hM-CSF level of 20 normal adults was 540 +/- 110 U/mL (range, 300 to 800 U/mL). The peak of hM-CSF measured by ELISA was identical to that measured by bioassay when semipurified CSF-HU was fractionated by reversed-phase high performance liquid chromatography (HPLC). This method detected two types of hM-CSF, which had approximate molecular weights of 85 Kd (CSF-HU) and 45 Kd in human serum and urine; the ratio of 85:45 Kd was very high in serum and the amounts of the two types were nearly equal in urine. After anticancer chemotherapy, the serum hM- CSF level of one half of the patients with hematological malignancy was elevated according to the reduction in neutrophil number, while it was almost in the normal range in the other half of the patients, indicating the possibility that anticancer chemotherapy damaged the hM- CSF-producing cells. This ELISA method may be useful for monitoring the serum hM-CSF level after anticancer chemotherapy.

scholarly journals Quantitation and identification of human monocytic colony-stimulating factor in human serum by enzyme-linked immunosorbent assay

Blood ◽  
1988 ◽  
Vol 72 (3) ◽  
pp. 886-892 ◽  
Author(s):  
T Hanamura ◽  
K Motoyoshi ◽  
K Yoshida ◽  
M Saito ◽  
Y Miura ◽  
...  
Keyword(s):  
Human Serum ◽  
Immunosorbent Assay ◽  
High Performance ◽  
Reversed Phase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Colony Stimulating Factor ◽  
Elisa System ◽  
Anticancer Chemotherapy ◽  
Average Serum ◽  
Stimulating Factor

An enzyme-linked immunosorbent assay (ELISA) system for the quantitation of human monocytic colony-stimulating factor (hM-CSF) was established, which was based on the “dual antibody immunometric sandwich” principle using horse and rabbit polyvalent antibodies against human urinary colony-stimulating factor (CSF-HU). The minimal detectable level of hM-CSF was 10 U/mL, and the assays showed good reproducibility. As measured by this method, the average serum hM-CSF level of 20 normal adults was 540 +/- 110 U/mL (range, 300 to 800 U/mL). The peak of hM-CSF measured by ELISA was identical to that measured by bioassay when semipurified CSF-HU was fractionated by reversed-phase high performance liquid chromatography (HPLC). This method detected two types of hM-CSF, which had approximate molecular weights of 85 Kd (CSF-HU) and 45 Kd in human serum and urine; the ratio of 85:45 Kd was very high in serum and the amounts of the two types were nearly equal in urine. After anticancer chemotherapy, the serum hM- CSF level of one half of the patients with hematological malignancy was elevated according to the reduction in neutrophil number, while it was almost in the normal range in the other half of the patients, indicating the possibility that anticancer chemotherapy damaged the hM- CSF-producing cells. This ELISA method may be useful for monitoring the serum hM-CSF level after anticancer chemotherapy.

scholarly journals Serum concentrations of granulocyte colony-stimulating factor in healthy term and preterm neonates and in those with various diseases including bacterial infections

Blood ◽  
1993 ◽  
Vol 82 (10) ◽  
pp. 3177-3182
Author(s):  
P Gessler ◽  
N Kirchmann ◽  
R Kientsch-Engel ◽  
N Haas ◽  
P Lasch ◽  
...  
Keyword(s):  
Bacterial Infections ◽  
Assay Method ◽  
Preterm Neonates ◽  
Enzyme Linked Immunosorbent Assay ◽  
Granulocyte Colony Stimulating Factor ◽  
Serum Concentrations ◽  
Colony Stimulating Factor ◽  
Csf Levels ◽  
Stimulating Factor

The neonate is uniquely susceptible to severe and overwhelming bacterial infections. One of the most important deficits in the neonatal host defense system seems to be a quantitative and qualitative deficiency of the myeloid and the phagocytic system. Future optimal therapy of neonatal sepsis may include the use of adjuvant immunologic therapy. Granulocyte colony-stimulating factor (G-CSF) has been shown to induce neutrophilia and to enhance mature effector neutrophil function. To evaluate the role of G-CSF with respect to infection, we examined serum levels of G-CSF in term and preterm neonates, using an enzyme-linked immunosorbent assay method. G-CSF levels in healthy neonates showed peak levels up to 7 hours after birth, followed by an increase in total neutrophil cell (TNC) counts. Both G-CSF levels determined between 4 and 7 hours after birth and peak TNC counts correlated with the gestational age of the neonates. The state of nutrition, maternal treatment with glucocorticoids, maternal infection and hypertension, and the mode of delivery influenced peak G-CSF levels. Neonates with signs of infection between 4 and 7 hours after birth had higher levels of G-CSF than did healthy neonates (1,312 +/- 396 pg/mL v 176 +/- 19 pg/mL). In conclusion, the presented results of serum concentrations of G-CSF in relation to TNC counts and various diseases suggests an important role of G-CSF in the regulation of granulopoiesis during the neonatal period.

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