Listeria monocytogenes is responsible for severe food-borne infections, but
the mechanisms by which bacteria cross the intestinal barrier are unknown.
Listeria monocytogenes expresses a surface protein, internalin, that inter
acts with a host receptor, E-cadherin, to promote entry into human epitheli
al cells. Murine E-cadherin, in contrast to guinea pig E-cadherin, does not
interact with internalin, excluding the mouse as a model for addressing in
ternalin function in vivo. In guinea pigs and transgenic mice expressing hu
man E-cadherin, internalin was found to mediate invasion of enterocytes and
crossing of the intestinal barrier. These results illustrate how relevant
animal models for human infections can be generated.