Listeria monocytogenes Internalin and E-cadherin: From Bench to Bedside
- Matteo Bonazzi1,2,3,
- Marc Lecuit4,5,6 and
- Pascale Cossart1,2,3
- 1Institut Pasteur, Unité des Interactions Bactéries-Cellules, Paris, F-75015 France
- 2Inserm, U604, Paris, F-75015 France
- 3INRA, USC2020, Paris, F-75015 France
- 4Institut Pasteur, Groupe Microorganismes et Barrières de l’Hôte, Paris, F-75015 France
- 5Inserm Avenir U604, Paris, F-75015 France
- 6Université Paris Descartes, Centre d’Infectiologie Necker-Pasteur, Service des Maladies Infectieuses et Tropicales, Hôpital Necker-Enfants malades, Assistance Publique-Hôpitaux de Paris, Paris, F-75015 France
- Correspondence: pcossart{at}pasteur.fr, mlecuit{at}pasteur.fr
Abstract
Listeria monocytogenes is a Gram-positive bacterium responsible for a severe infection associated with different clinical features (gastroenteritis, meningoencephalitis, and abortion in pregnant women). These pathologies are caused by the unusual capacity of the bacterium to cross three host barriers during infection and to invade nonphagocytic cells. To invade host cells, Listeria uses two proteins, InlA and InlB, which have specific receptors on the host-cell surface, E-cadherin and Met, respectively. Here, we discuss the specificity of the InlA–E-cadherin interaction, the signaling cascade activated on E-cadherin engagement by InlA, and the role of InlA and E-cadherin in the breaching of host barriers and the dissemination of the infection.
Footnotes
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Editors: W. James Nelson and Elaine Fuchs
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Additional Perspectives on Cell Junctions available at www.cshperspectives.org
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