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1
*
Pharmazentrum Frankfurt and
Second Department of Medicine, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany
IL-18 and IL-18 binding protein (IL-18BP) are two newly described
opponents in the cytokine network. Local concentrations of these two
players may determine biological functions of IL-18 in the context of
inflammation, infection, and cancer. As IL-18 appears to be involved in
the pathogenesis of Crohn’s disease and may modulate tumor growth, we
investigated the IL-18/IL-18BPa system in the human colon
carcinoma/epithelial cell line DLD-1. In this study, we report that
IFN-
induces expression and release of IL-18BPa from DLD-1 cells.
mRNA induction and secretion of IL-18BPa immunoreactivity were
associated with an activity that significantly impaired release of
IFN- by IL-12/IL-18-stimulated PBMC. Inducibility of IL-18BPa by
IFN- was also observed in LoVo, Caco-2, and HCT116 human colon
carcinoma cell lines and in the human keratinocyte cell line HaCaT.
Induction of IL-18BPa in colon carcinoma/epithelial cell lines was
suppressed by coincubation with sodium butyrate. IFN--mediated
IL-18BPa and its suppression by sodium butyrate were confirmed in organ
cultures of intestinal colonic biopsy specimens. In contrast, sodium
butyrate did not modulate expression of IL-18. The present data suggest
that IFN- may limit biological functions of IL-18 at sites of
colonic immune activation by inducing IL-18BPa production.
Down-regulation of IL-18BPa by sodium butyrate suggests that
reinforcement of local IL-18 activity may contribute to actions of this
short-chain fatty acid in the colonic
microenvironment.
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