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CF Lai and H Baumann
Department of Molecular and Cellular Biology, Roswell Park Cancer
Institute, Buffalo, NY 14263, USA.
Interleukin-1 (IL-1) is a proinflammatory cytokine that participates in the
activation of the acute-phase plasma protein genes in hepatic cells during
infection and injury. In human hepatoma HepG2 and Hep3B cells, IL-1 beta
induced production of the granulocyte colony-stimulating factor (G-CSF) in
a dose-dependent manner. Activation of G-CSF gene expression was an early
and transient response. In HepG2 cells, G-CSF mRNA was strongly upregulated
2 hours after IL-1 beta treatment and returned to the pretreatment level by
6 hours. The secreted G-CSF was biologically active, as shown by the
induction of gene transcription through the G-CSF receptor. Maximal G-CSF
activity released to culture medium occurred after 8 hours. Previous
studies have shown that liver expression of G-CSF was augmented in mice
challenged by inflammatory stimuli. Our data suggest that IL-1 beta
mediates, at least in part, this cytokine activation program in parenchymal
cells and that liver- derived G-CSF may contribute to the regulation of
hematopoiesis during the acute-phase response.
This article has been cited by other articles:
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| Copyright © 1996 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
