Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Bacterial Proteins / metabolism*
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Bacterial Translocation
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Cadherins / genetics
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Cadherins / metabolism*
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Carrier Proteins / genetics
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Colony Count, Microbial
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Disease Models, Animal*
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Enterocytes / metabolism
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Enterocytes / microbiology*
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Fatty Acid-Binding Protein 7
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Fatty Acid-Binding Proteins
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Guinea Pigs
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Humans
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Intestinal Mucosa / microbiology
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Intestinal Mucosa / pathology
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Intestine, Small / microbiology
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Intestine, Small / pathology
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Listeria monocytogenes / growth & development
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Listeria monocytogenes / metabolism
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Listeria monocytogenes / pathogenicity*
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Listeriosis / microbiology*
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Listeriosis / pathology
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Liver / microbiology
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Liver / pathology
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Lymph Nodes / microbiology
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Lymph Nodes / pathology
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Male
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Mice
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Mice, Transgenic
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Neoplasm Proteins*
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Nerve Tissue Proteins*
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Promoter Regions, Genetic
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Spleen / microbiology
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Spleen / pathology
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Transgenes
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Tumor Suppressor Proteins*
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Virulence
Substances
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Bacterial Proteins
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Cadherins
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Carrier Proteins
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FABP7 protein, human
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Fabp5 protein, mouse
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Fabp7 protein, mouse
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Fatty Acid-Binding Protein 7
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Fatty Acid-Binding Proteins
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Neoplasm Proteins
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Nerve Tissue Proteins
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Tumor Suppressor Proteins
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internalin protein, Bacteria