Enterohemorrhagic Escherichia coli O157:H7 (EHEC) is an important food-borne pathogen. While the molecular mechanisms governing E. coli O157:H7 pathogenesis have been intensively investigated, the role of host factors has received less attention. In this study, we tested the hypothesis that the enteric catecholamines norepinephrine (NE) and dopamine (DA) modulate interactions of the cecal mucosa with E. coli O157:H7. Full-thickness sheets of murine cecum were mounted in Ussing chambers and short circuit current and tissue electrical conductance were periodically determined to assess active transepithelial ion transport and ionic permeability, respectively. Neurochemicals and stationary-phase E. coli O157:H7 were exposed respectively to the contraluminal and luminal aspects of the mucosa. Epithelial adherence of E. coli O157:H7 was quantified by a bacterial adhesion assay after 90 min of luminal E. coli O157:H7 exposure. DA and NE increased E. coli O157:H7 adherence relative to untreated control tissues at 50% effective concentrations of 3.8 microM and 4.2 microM respectively. Pretreatment of tissues with either the alpha-adrenergic antagonist phentolamine or the beta-adrenergic antagonist propranolol prevented the action of NE. The effect of DA was prevented by the dopamine antagonist haloperidol. The drugs did not impair tissue viability or transepithelial conductance. The present findings suggest that enteric catecholamines modulate E. coli O157:H7 adherence to the cecal epithelium. Conditions associated with elevated catecholamine release, such as stress exposure, may influence host susceptibility to E. coli O157:H7 infection.