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Blood, Vol. 93 No. 4 (February 15), 1999:
pp. 1299-1307
Interleukin-4 (IL-4) and IL-13 Enhance the Effect of IL-1 on
Production of IL-1 Receptor Antagonist by Human Primary Hepatocytes and
Hepatoma HepG2 Cells: Differential Effect on C-Reactive Protein
Production
Cem Gabay,
Brandon Porter,
Denis Guenette,
Bahri Billir, and
William P. Arend
From the Division of Rheumatology and the Division of
Gastroenterology, Department of Medicine, University of Colorado Health
Sciences Center, Denver, CO 80262.
Interleukin-1 receptor antagonist (IL-1Ra) is produced by
hepatocytes with characteristics of an acute-phase protein. To examine the role of IL-4 and IL-13 in production of IL-1Ra, human primary hepatocytes and HepG2 human hepatoma cells were cultured in the presence of IL-4 or IL-13 in combination with IL-1 and/or
IL-6. The results indicated that both IL-4 and IL-13 amplified the
stimulatory effect of IL-1 on production of IL-1Ra protein and
messenger RNA (mRNA) by both human primary hepatocytes and HepG2 cells. IL-1Ra refers to three different peptides, one secreted (sIL-1Ra) and
two intracellular (icIL-1RaI and icIL-1RaII), derived from the same
gene. sIL-1Ra and icIL-1RaI are the products of two different mRNA,
whereas icIL-1RaII is synthesized by alternative translation initiation
mainly from sIL-1Ra mRNA. Our results show that both sIL-1Ra and
icIL-1RaII, but not icIL-1RaI, are produced by HepG2 cells and human
hepatocytes. Transient transfection experiments as well as mRNA
stability studies indicated that IL-4 stimulated sIL-1Ra production
primarly at the level of transcription. Gel retardation assays showed
that IL-4 induced the formation of a STAT6-DNA complex with a STAT6
binding element within the sIL-1Ra promoter, but had no effect on
IL-1-induced NF- B binding activity. In contrast to IL-1Ra,
production of C-reactive protein by human primary hepatocytes was
stimulated by IL-6 and decreased by the addition of IL-4.
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