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

被引:460
作者
Lecuit, M
Vandormael-Pournin, S
Lefort, J
Huerre, M
Gounon, P
Dupuy, C
Babinet, C
Cossart, P [1 ]
机构
[1] Inst Pasteur, Unite Interact Bacteries Cellules, CNRS, Unite Rech Associee 1960, F-75724 Paris 15, France
[2] Inst Pasteur, Unite Biol Dev, CNRS, Unite Rech Associee 1960, F-75724 Paris, France
[3] Inst Pasteur, Unite Pharmacol Cellulaire, F-75724 Paris 15, France
[4] Inst Pasteur, Unite Histopathol, F-75724 Paris 15, France
[5] Inst Pasteur, Stn Cent Microscopie Electron, F-75724 Paris 15, France
关键词
D O I
10.1126/science.1059852
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1722 / 1725
页数:4
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