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30. Supported by grants from NIH. R.T.M. is an investi-
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22 February 2001; accepted 23 April 2001
A Transgenic Model for
Listeriosis: Role of Internalin in
Crossing the Intestinal Barrier
Marc Lecuit,1 Sandrine Vandormael-Pournin,2 Jean Lefort,3
Michel Huerre,4 Pierre Gounon,5 Catherine Dupuy,1
Charles Babinet,2 Pascale Cossart1*
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 interacts with a host
receptor, E-cadherin, to promote entry into human epithelial cells. Murine E-
cadherin, in contrast to guinea pig E-cadherin, does not interact with internalin,
excluding the mouse as a model for addressing internalin function in vivo. In guinea
pigs and transgenic mice expressing human 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.
Understanding how bacteria cross the intesti-
nal barrier is a key issue in the study of
foodborne diseases. Listeria monocytogenes
causes listeriosis, an infection characterized
by bacterial dissemination from the intestinal
lumen to the central nervo