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Granulocyte-macrophage colony-stimulating factor expression by human
fibroblasts is both upregulated and subsequently downregulated by
interleukin-1
RR Patil and RF Borch
Department of Pharmacology, University of Rochester, NY 14642.
Interleukin-1 (IL-1) treatment of human WI-38 lung fibroblasts results in
granulocyte-macrophage colony-stimulating factor (GM-CSF) expression as
well as a delayed increase in prostaglandin E2 (PGE2) production that
closely correlates with the decline of GM-CSF mRNA levels. Pretreatment
with PGE2 reduces the IL-1 induced GM-CSF mRNA and protein expression to
10% to 15% of control values at concentrations of PGE2 that are
endogenously produced after IL-1 stimulation. Inhibition of PGE2 synthesis
by indomethacin prolongs the IL-1 induced GM-CSF mRNA expression and
increases the cumulative GM-CSF protein secretion. Exposure of WI-38
fibroblasts to PGE2 results in an increase in intracellular cyclic
adenosine monophosphate (cAMP) levels. The inhibition of GM-CSF expression
by PGE2 can be mimicked by stable cAMP analogs as well as cAMP elevating
agents such as cholera toxin, forskolin, and isobutylmethylxanthine. Thus
the inhibition exerted by PGE2 is mediated via cAMP. Taken together, these
results suggest that IL-1 stimulation of human fibroblasts provides not
only the upregulatory signal for GM-CSF expression but also a delayed and
indirect downregulatory signal that serves to limit GM-CSF expression in
the continued presence of IL-1.
Volume 85,
Issue 1,
pp. 80-86,
01/01/1995
Copyright © 1995 by The American Society of Hematology
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