Enteric bacterial pathogens often increase intestinal Cl⁻ secretion. Enteropathogenic Escherichia coli(EPEC) does not stimulate active ion secretion. In fact, EPEC infection decreases net ion transport in response to classic secretagogues. This has been presumed to reflect diminished Cl⁻ secretion. The aim of this study was to investigate the influence of EPEC infection on specific intestinal epithelial ion transport processes. T84 cell monolayers infected with EPEC were used for these studies. EPEC infection significantly decreased short-circuit current (I _sc) in response to carbachol and forskolin, yet¹²⁵I efflux studies revealed no difference in Cl⁻ channel activity. There was also no alteration in basolateral K⁺ channel or Na⁺-K⁺-2Cl⁻cotransport activity. Furthermore, net³⁶Cl⁻flux was not decreased by EPEC. No alterations in either K⁺ or Na⁺ transport could be demonstrated. Instead, removal of basolateral bicarbonate from uninfected monolayers yielded anI _sc response approximating that observed with EPEC infection, whereas bicarbonate removal from EPEC-infected monolayers further diminishedI _sc. These studies suggest that the reduction in stimulatedI _sc is not secondary to diminished Cl⁻secretion. Alternatively, bicarbonate-dependent transport processes appear to be perturbed.