Abstract
The food-borne pathogen Listeria monocytogenes is able to colonize the human gastro-intestinal tract and subsequently cross the intestinal barrier. Thus, for L. monocytogenes to become virulent, it must survive the low pH of the stomach, high bile concentrations in the small intestine, and invade the epithelial cells. In this study, we show that RecA, which is an important factor in DNA repair and the activator of the SOS response, contributes to the resistance against acid and bile and to the ability of L. monocytogenes to adhere and invade human intestine epithelial cells. Activation of recA was shown with a promoter reporter after exposure to low pH and high bile concentrations and during adhesion and invasion of Caco-2 intestinal epithelial cells. Furthermore, an in-frame recA deletion mutant showed reduced survival after exposure to low pH and high bile concentrations. This mutant also showed a deficiency in adhesion and invasion of Caco-2 cells. These results suggest that RecA may contribute to the colonization of the human gastro-intestinal tract and crossing of the intestinal barrier.
Published Version
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