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1 Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
2 Unilever Health Institute, Vlaardingen, Netherlands Antilles
* To whom correspondence should be addressed. E-mail: bienens{at}mcmaster.ca.
The intestinal mucosa is in a constant state of controlled inflammation, but the processes whereby this occurs are poorly understood. The aims of this study were to look at the role of IL-10 and NGF in intestinal epithelial cell regulation. The human colon epithelial cell line T84, HT-29 and CACO-2 were used. RT-PCR, flow cytometry analysis and immunohistochemistry were applied to measure the cytokine changes in epithelial cells induced by recombinant cholera toxin and its B subunit , IL-10 and NGF. Cholera toxin B subunit caused selective dose dependent increased mRNA for IL-10 in T84 cells and the protein in T84, HT-29 and CACO-2 cells. IL-10 dose dependently selectively increased NGF mRNA in T84 cells and intracellular protein synthesis in all 3 epithelial cell lines. The effect of NGF was reciprocal, selective and dose dependent since it increased mRNA for IL-10 and IL-10 synthesis. Our results suggest that the epithelium may actively participate in downregulation through innate mechanisms involving IL-10 and NGF. The reciprocal interaction suggests for the first time that NGF may be involved in local downregulation by mucosal epithelium, and thus may play a potent protective role in response to injury, by prevention of undue inflammation.
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