Mapping of the antibody- and receptor-binding domains of granulocyte colony-stimulating factor using and optical biosensor Comparison with enzyme-linked immunosorbent assay competition studies

1993 ◽  
Vol 646 (1) ◽  
pp. 159-168 ◽  
Author(s):  
Edouard Nice ◽  
Judith Layton ◽  
Louis Fabri ◽  
Ulf Hellman ◽  
Ake Engstrom ◽  
...  
1995 ◽  
Vol 3 (4) ◽  
pp. 140-144 ◽  
Author(s):  
B. Denise Raynor ◽  
Penny Clark ◽  
Patrick Duff

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.


1997 ◽  
Vol 6 (8) ◽  
pp. 1787-1787
Author(s):  
Dennis C. Young ◽  
Qi-Lin Cheng ◽  
Jinzhao Hou ◽  
David J. Matthews ◽  
Hangjun Zhan

1997 ◽  
Vol 6 (6) ◽  
pp. 1228-1236 ◽  
Author(s):  
Dennis C. Young ◽  
Qi-Lin Cheng ◽  
Jinzhao Hou ◽  
David J. Matthews ◽  
Hangjun Zhan

Blood ◽  
1993 ◽  
Vol 82 (10) ◽  
pp. 3177-3182 ◽  
Author(s):  
P Gessler ◽  
N Kirchmann ◽  
R Kientsch-Engel ◽  
N Haas ◽  
P Lasch ◽  
...  

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.


Blood ◽  
1994 ◽  
Vol 84 (3) ◽  
pp. 789-794 ◽  
Author(s):  
BR Avalos ◽  
VC Broudy ◽  
SK Ceselski ◽  
BJ Druker ◽  
JD Griffin ◽  
...  

A decrease in responsiveness to granulocyte colony-stimulating factor (G-CSF) has been implicated in the pathophysiology of cyclic hematopoiesis. Using the canine model of cyclic neutropenia, we examined the response of neutrophil precursors to G-CSF in vitro and G- CSF receptor expression in neutrophils from grey collie dogs to determine whether the abnormal response observed to G-CSF in vivo in this disorder is present at the level of the progenitor cell and is caused by defective G-CSF receptor expression. Bone marrow mononuclear cells from grey collie dogs required sevenfold higher G-CSF concentrations than normal dog cells to achieve half-maximal colony growth [56 pmol/L v 8 pmol/L). Receptor binding assays with 125I- labeled G-CSF and Scatchard analyses of the equilibrium binding data were consistent with expression of a single class of high-affinity receptors for G-CSF on neutrophils from both normal dogs and grey collies with similar receptor numbers (56 to 446 sites/cell v 78 to 199 sites/cell) and binding affinities (28 to 206 pmol/L v 84 to 195 pmol/L). Chemical cross-linking studies identified a G-CSF binding protein of approximately 120 kD on neutrophils from grey collies, similar in size to that on normal dog neutrophils. No abnormal G-CSF receptor mRNA transcripts were detected in neutrophils from grey collie dogs by Northern blot analysis. Treatment of both normal and grey collie neutrophils with G-CSF rapidly induced tyrosine phosphorylation of an 80-kD protein that behaved like canine c-rel. These results demonstrate that the abnormal responsiveness to G-CSF in canine cyclic hematopoiesis is present in neutrophil precursors and is not associated with demonstrable alterations in the number, binding affinity, or overall size of the G-CSF receptor in neutrophils, or with defective tyrosine phosphorylation of p80. These data suggest that cyclic hematopoiesis is caused by a defect in the G-CSF signal transduction pathway at a point distal to G-CSF receptor binding that does not involve the early biochemical events leading to p80 tyrosine phosphorylation.


Sign in / Sign up

Export Citation Format

Share Document