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(American Journal of Pathology. 2003;163:1969-1977.)
© 2003 American Society for Investigative Pathology

Interferon- Increases hPepT1-Mediated Uptake of Di-Tripeptides Including the Bacterial Tripeptide fMLP in Polarized Intestinal Epithelia

Marion Buyse^*, Laetitia Charrier^*, Shanthi Sitaraman^*, Andrew Gewirtz and Didier Merlin^*

From the Department of Medicine,^* Division of Digestive Diseases, and the Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia

Interferon- causes a global phenotypic switch in intestinal epithelial function, in which enterocytes become immune accessory cells. The phenotypic switch is characterized by a down-regulation of membrane transporters and up-regulation of immune accessory molecules in intestinal epithelial cells. However, the effect of interferon- on the intestinal epithelia di-tripeptide hPepT1 transporter has not been investigated. In this study we demonstrate that 1) interferon- increases di-tripeptide uptake in dose- and time-dependent manner in model intestinal epithelia (Caco-2 BBE cell monolayers), 2) the increase in di-tripeptides induced by interferon- is hPepT1 mediated, 3) interferon- does not affect the hPept1 expression at the mRNA and protein levels 4) interferon- increases the intracellular pH and consequently enhances the H⁺-electrochemical gradient across apical plasma membrane in model intestinal epithelia (Caco2-BBE monolayers). We suggest that interferon- could increase the hPepT1 mediated di-tripeptides uptake in inflamed epithelial cells. Under these conditions, interferon- will increase the intracellular amount of such diverse prokaryotic and eucaryotic small di-tripeptides in inflamed epithelial cells. The intracellular accumulation of such di-tripeptides may be important in enterocytes becoming immune accessory cells.

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