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Am J Physiol Cell Physiol (February 6, 2002). doi:10.1152/ajpcell.00113.2001
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Articles in PresS, published online ahead of print February 6, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00113.2001
Submitted on March 5, 2001
Accepted on January 15, 2002

MAP Kinases contribute to IL-8 secretion by intestinal epithelial cells via a post-transcriptional mechanism

Humberto B Jijon1*, William J Panenka1, Karen L Madsen2, and Howard G Parsons1

1 Gastrointestinal Research Group, University of Calgary, Calgary, AB, USA
2 Division of Gastroenterology, University of Alberta, Edmonton, AB, Canada

* To whom correspondence should be addressed. E-mail: hjijon{at}ualberta.ca.

The intracellular pathways which regulate intestinal epithelial gene expression are poorly understood. In this study we examined the roles of Extracellular Signal-Regulated Kinase (ERK) and p38 in the expression of interleukin 8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1) using the human intestinal cell line HT-29. HT-29 cells were treated with tumor necrosis factor-alpha (TNF-{alpha}) in the presence or absence of ERK and p38 pathway inhibitors. TNF-{alpha} treatment resulted in increased IL-8 and ICAM-1 protein and mRNA synthesis, increased ERK and p38 activity and activation of the transcription factors AP-1 and NF-{kappa}B. Inhibition of the ERK and p38 pathways attenuated IL-8 secretion but did not alter ICAM-1 expression. Further, AP-1 and NF-{kappa}B DNA-binding were not affected by ERK and p38 inhibition. In contrast, ERK and p38 inhibition resulted in the accelerated degradation of the IL-8 mRNA, suggesting that in HT-29 cells, p38 and ERK contribute to TNF-{alpha}-stimulated IL-8 secretion by intestinal epithelial cells via a post-transcriptional mechanism which involves stabilization of the IL-8 transcript.




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