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© Pierre Gounon
Entrée de Listeria dans une cellule épithéliale (Grossissement X 10000). Image colorisée.
Publication : Science (New York, N.Y.)

A transgenic model for listeriosis: role of internalin in crossing the intestinal barrier.

Team: Bacteria-Cell Interactions
Team: Biology of infection
Member: Pascale Cossart
Member: Marc Lecuit
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Science (New York, N.Y.) - 01 Jun 2001

Lecuit M, Vandormael-Pournin S, Lefort J, Huerre M, Gounon P, Dupuy C, Babinet C, Cossart P,

Link to Pubmed [PMID] – 11387478

Science 2001 Jun; 292(5522): 1722-5

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.