Barrett's esophagus (BE) is considered to be the most severe complication of gastro-esophageal reflux disease (GERD), in which the prolonged, repetitive episodes of combined acidic and biliary reflux result in the replacement of the squamous esophageal lining by columnar epithelium. Therefore, acid extruding mechanisms of esophageal epithelial cells (EECs) may play an important role in the defence. Our aim was to identify the presence of acid/base transporters on EECs and to investigate the effect of bile acids on their expressions and functions. Human EEC lines (CP-A and CP-D) was acutely exposed to bile acid cocktail (BAC) and the changes in intracellular pH (pHi) and Ca2+ concentration ([Ca2+]i) were measured by microfluorometry. mRNA and protein expression of ion transporters were investigated by RT-PCR, Western Blot and immunohistochemistry. We have identified the presence of Na+/H+ exchanger (NHE), Na+/HCO3- cotransporter (NBC) and a Cl- dependent HCO3- secretory mechanism in CP-A and CP-D cells. Acute administration of BAC stimulated HCO3- secretion in both cell lines and the NHE activity in CP-D cells by an IP3-dependent calcium release. Chronic administration of BAC to EECs increased the expression of ion transporters compared to non-treated cells. Similar expression pattern was observed in biopsy samples from BE compared to normal epithelium. We have shown that acute administration of bile acids differently alters ion transport mechanisms of EECs, whereas chronic exposure to bile acids increases the expression of acid/base transporters. We speculate that these adaptive processes of EECs, represent an important mucosal defence against the bile acid-induced epithelial injury.