TY - JOUR
T1 - Modulation of receptors for the colony-stimulating factor, CSF-1, by bacterial lipopolysaccharide and CSF-1
AU - Guilbert, L. J.
AU - Stanley, E. R.
N1 - Funding Information:
This work was supportebdy Grant CA 26504f romthe NationaCl ancerI nstitute, a grant from the AECOM Cancer Center Core and a grant from the Kroc Foundation.
PY - 1984/10/12
Y1 - 1984/10/12
N2 - The ability of the mononuclear phagocyte-specific colony-stimulating factor, CSF-1, to down-regulate its receptor on peritoneal exudate macrophages (PEM) was examined. Because of the essentially irreversible binding of CSF-1 to its receptor at 2°C, unoccupied cell surface receptors could be measured by rapidly cooling PEM to 2°C and determining the amount of 125I-CSF-1 bound at this temperature. On incubation with 125I-CSF-1 at 37°C more receptors were lost than could be accounted for by 125I-CSF-1 binding. This receptor loss, apparently caused by CSF-1 itself, was shown to be due in large part to the presence of contaminating lipopolysaccharide (LPS), which at 10 ng/ml was by itself able to cause complete loss of the CSF-1 receptors. LPS also induced loss of the insulin receptor by PEM. LPS did not cause apparent CSF-1 receptor loss by binding to the receptor or by stimulating the release of CSF-1 or substances which complete for the binding of 125I-CSF-1 to the receptor. However, LPS did stimulate release of factos by LPS responsive (C3H/HeN) PEM which caused CSF-1 receptor loss by LPS non-responsive (C3H/HeJ) PEM. In the absence of LPS induced effects, incubation of 125I-CSF-1 with PEM at 37°C resulted in down-regulation of the CSF-1 receptors. The number of CSF-1 receptor sites down-regulated corresponded to the number of CSF-1 molecules that were cell-associated plus the number that were intracellularly degraded and released.
AB - The ability of the mononuclear phagocyte-specific colony-stimulating factor, CSF-1, to down-regulate its receptor on peritoneal exudate macrophages (PEM) was examined. Because of the essentially irreversible binding of CSF-1 to its receptor at 2°C, unoccupied cell surface receptors could be measured by rapidly cooling PEM to 2°C and determining the amount of 125I-CSF-1 bound at this temperature. On incubation with 125I-CSF-1 at 37°C more receptors were lost than could be accounted for by 125I-CSF-1 binding. This receptor loss, apparently caused by CSF-1 itself, was shown to be due in large part to the presence of contaminating lipopolysaccharide (LPS), which at 10 ng/ml was by itself able to cause complete loss of the CSF-1 receptors. LPS also induced loss of the insulin receptor by PEM. LPS did not cause apparent CSF-1 receptor loss by binding to the receptor or by stimulating the release of CSF-1 or substances which complete for the binding of 125I-CSF-1 to the receptor. However, LPS did stimulate release of factos by LPS responsive (C3H/HeN) PEM which caused CSF-1 receptor loss by LPS non-responsive (C3H/HeJ) PEM. In the absence of LPS induced effects, incubation of 125I-CSF-1 with PEM at 37°C resulted in down-regulation of the CSF-1 receptors. The number of CSF-1 receptor sites down-regulated corresponded to the number of CSF-1 molecules that were cell-associated plus the number that were intracellularly degraded and released.
KW - colony-stimulating factor (CSF-1)
KW - endotoxin
KW - growth factor receptors
KW - lipopolysaccharide
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U2 - 10.1016/0022-1759(84)90027-9
DO - 10.1016/0022-1759(84)90027-9
M3 - Article
C2 - 6092475
AN - SCOPUS:0021207834
SN - 0022-1759
VL - 73
SP - 17
EP - 28
JO - Journal of Immunological Methods
JF - Journal of Immunological Methods
IS - 1
ER -