Interleukin-1 beta induces production of granulocyte colony-stimulating factor in human hepatoma cells

Blood. 1996 May 15;87(10):4143-8.

Abstract

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.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acute-Phase Reaction / chemically induced*
  • Culture Media, Conditioned / chemistry
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Genetic Vectors
  • Granulocyte Colony-Stimulating Factor / biosynthesis*
  • Hematoma / metabolism*
  • Hematoma / pathology
  • Humans
  • Interleukin-1 / pharmacology*
  • Interleukin-6 / pharmacology
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / pathology
  • Neoplasm Proteins / biosynthesis*
  • RNA, Messenger / biosynthesis
  • RNA, Neoplasm / biosynthesis
  • Receptors, Granulocyte Colony-Stimulating Factor / genetics
  • Receptors, Granulocyte Colony-Stimulating Factor / metabolism
  • Recombinant Fusion Proteins / metabolism
  • Recombinant Fusion Proteins / pharmacology
  • Transcription, Genetic
  • Transfection
  • Tumor Cells, Cultured / drug effects

Substances

  • Culture Media, Conditioned
  • Interleukin-1
  • Interleukin-6
  • Neoplasm Proteins
  • RNA, Messenger
  • RNA, Neoplasm
  • Receptors, Granulocyte Colony-Stimulating Factor
  • Recombinant Fusion Proteins
  • Granulocyte Colony-Stimulating Factor