Enteropathogenic Escherichia coli (EPEC) is recognized as an important intestinal pathogen that frequently causes acute and persistent
diarrhea in humans and animals. The use of probiotic bacteria to prevent
diarrhea is gaining increasing interest. The probiotic E. coli strain Nissle 1917 (
EcN) is known to be effective in the treatment of several
gastrointestinal disorders. While both in vitro and in vivo studies have described strong inhibitory effects of
EcN on enteropathogenic bacteria, including pathogenic E. coli, the underlying molecular mechanisms remain largely unknown. In this study, we examined the inhibitory effect of
EcN on
infections of porcine intestinal epithelial cells with atypical enteropathogenic E. coli (aEPEC) with respect to single
infection steps, including adhesion, microcolony formation, and the attaching and effacing phenotype. We show that
EcN drastically reduced the
infection efficiencies of aEPEC by inhibiting bacterial adhesion and growth of microcolonies, but not the attaching and effacing of adherent bacteria. The inhibitory effect correlated with
EcN adhesion capacities and was predominantly mediated by F1C fimbriae, but also by H1 flagella, which served as bridges between
EcN cells. Furthermore,
EcN seemed to interfere with the initial adhesion of aEPEC to host cells by secretion of inhibitory components. These components do not appear to be specific to
EcN, but we propose that the strong adhesion capacities enable
EcN to secrete sufficient local concentrations of the inhibitory factors. The results of this study are consistent with a mode of action whereby
EcN inhibits secretion of virulence-associated
proteins of EPEC, but not their expression.