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Prostaglandin E₂ Stimulates IL-8 Gene Expression in Human Colonic Epithelial Cells by a Posttranscriptional Mechanism¹

Institute of Parasitology, McGill University, Ste. Anne de Bellevue, Quebec, Canada

Intestinal mucosal epithelial cells produce IL-8, a neutrophil chemoattractant that contributes to mucosal inflammation in various infectious and inflammatory diseases. However, the mediators involved and the molecular regulation of IL-8 production are poorly understood. As PGE₂ is central in gut inflammation and modulates a variety of mucosal epithelial cell functions, we determined whether PGE₂ can affect the expression of IL-8. Exogenous PGE₂ induced the accumulation of IL-8 mRNA and protein production in a dose- and time-dependent manner in T84 human colonic epithelial cells. Forskolin and dibutyryl cAMP, which increase intracellular cAMP, stimulated IL-8 in a fashion similar to that of PGE₂. PGE₂ and PGE₂ receptor agonists coupling through EP₄ receptors elevated intracellular cAMP and up-regulated IL-8 mRNA expression by activating protein kinase A. Unlike PMA, PGE₂ and forskolin did not increase IL-8 gene transcription. However, PGE₂, forskolin, and PMA enhanced the stability of IL-8 mRNA transcripts, suggesting the involvement of posttranscriptional regulation. Chloramphenicol acetyltransferase reporter gene transfection studies confirmed the presence of a PGE₂ responsive cis-element(s) in the IL-8 3' untranslated region. Furthermore, dexamethasone inhibited PGE₂-, forskolin-, and dibutyryl cAMP-induced, but not PMA-induced, IL-8 protein production. These results highlight a novel role for PGE₂ in up-regulating IL-8 gene expression by colonic epithelial cells, which may contribute to exacerbation of inflammation in the gastrointestinal tract.

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