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Letter

Nature 455, 1114-1118 (23 October 2008) | doi:10.1038/nature07303; Received 19 March 2008; Accepted 30 July 2008; Published online 17 September 2008

Open Innovation Challenges

Conjugated action of two species-specific invasion proteins for fetoplacental listeriosis

Olivier Disson1,2,10, Solène Grayo1,2,3,10, Eugénie Huillet4,5,6,10, Georgios Nikitas1,2, Francina Langa-Vives7, Olivier Dussurget4,5,6, Marie Ragon3, Alban Le Monnier3, Charles Babinet8,11, Pascale Cossart4,5,6 & Marc Lecuit1,2,3,9

  1. Institut Pasteur, Groupe Microorganismes et Barrières de l'Hôte, Unité des Interactions Bactéries-Cellules, F-75015 Paris, France
  2. Inserm Avenir U604, F-75015 Paris, France
  3. Institut Pasteur, Centre National de Référence des Listeria, F-75015 Paris, France
  4. Institut Pasteur, Unité des Interactions Bactéries-Cellules, F-75015 Paris, France
  5. Inserm U604, F-75015 Paris, France
  6. INRA USC2020, F-75015 Paris, France
  7. Institut Pasteur, Centre d'Ingénierie Génétique Murine, F-75015 Paris, France
  8. Institut Pasteur, Unité de Biologie du Développement, F-75015 Paris, France
  9. Centre d'Infectiologie Necker-Pasteur, Service des Maladies Infectieuses et Tropicales, Hôpital Necker-Enfants malades, Assistance Publique-Hôpitaux de Paris, Université Paris Descartes, F-75015 Paris, France
  10. These authors contributed equally to this work.
  11. Deceased.

Correspondence to: Marc Lecuit1,2,3,9 Correspondence and requests for materials should be addressed to M.L. (Email: mlecuit@pasteur.fr).

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The ability to cross host barriers is an essential virulence determinant of invasive microbial pathogens. Listeria monocytogenes is a model microorganism that crosses human intestinal and placental barriers, and causes severe maternofetal infections by an unknown mechanism1. Several studies have helped to characterize the bacterial invasion proteins InlA and InlB2. However, their respective species specificity has complicated investigations on their in vivo role3, 4. Here we describe two novel and complementary animal models for human listeriosis: the gerbil, a natural host for L. monocytogenes, and a knock-in mouse line ubiquitously expressing humanized E-cadherin. Using these two models, we uncover the essential and interdependent roles of InlA and InlB in fetoplacental listeriosis, and thereby decipher the molecular mechanism underlying the ability of a microbe to target and cross the placental barrier.