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Infection and Immunity, January 2006, p. 663-672, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.663-672.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Invasion of the Placenta during Murine Listeriosis

Alban Le Monnier,1,2,3 Olivier F. Join-Lambert,1,2,3 Francis Jaubert,1,3,4 Patrick Berche,1,2,3 and Samer Kayal1,2,3*

Faculté de Médecine, Université René Descartes Paris-5, U-570 INSERM, 156 rue de Vaugirard, 75730 Paris Cedex 15,1 INSERM Paris,2 Assistance Publique-Hôpitaux de Paris, Paris,3 Département d'Anatomie Pathologique, Hôpital Necker-Enfants Malades, 149 rue de Sèvres, 75015 Paris, France4

Received 27 July 2005/ Returned for modification 1 September 2005/ Accepted 2 October 2005

Feto-placental infections due to Listeria monocytogenes represent a major threat during pregnancy, and the underlying mechanisms of placental invasion remain poorly understood. Here we used a murine model of listeriosis (pregnant mice, infected at day 14 of gestation) to investigate how this pathogen invades and grows within the placenta to ultimately infect the fetus. When L. monocytogenes is injected intravenously, the invasion of the placenta occurs early after the initial bacteremia, allowing the placental growth of the bacteria, which is an absolute requirement for vertical transmission to the fetus. Kinetically, bacteria first target the cells lining the central arterial canal of the placenta, which stain positively with cytokeratin, demonstrating their fetal trophoblast origin. Bacteria then disseminate rapidly to the other trophoblastic structures, like syncytiotrophoblast cells lining the villous core in the labyrinthine zone of placenta. Additionally, we found that an inflammatory reaction predominantly constituted of polymorphonuclear cells occurs in the villous placenta and participates in the control of infection. Altogether, our results suggest that the infection of murine placenta is dependent, at the early phase, on circulating bacteria and their interaction with endovascular trophoblastic cells. Subsequently, the bacteria spread to the other trophoblastic cells before crossing the placental barrier.

* Corresponding author. Mailing address: INSERM U-570, Faculté de Médecine 156 rue de Vaugirard, 75730 Paris Cedex 15, France. Phone: 33-1-40-61-55-93. Fax: 33-1-40-61-55-92. E-mail: kayal{at}necker.fr.

Editor: D. L. Burns

Infection and Immunity, January 2006, p. 663-672, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.663-672.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Pejcic-Karapetrovic, B., Gurnani, K., Russell, M. S., Finlay, B. B., Sad, S., Krishnan, L. (2007). Pregnancy Impairs the Innate Immune Resistance to Salmonella typhimurium Leading to Rapid Fatal Infection. J. Immunol. 179: 6088-6096 [Abstract] [Full Text]  
  • Le Monnier, A., Autret, N., Join-Lambert, O. F., Jaubert, F., Charbit, A., Berche, P., Kayal, S. (2007). ActA Is Required for Crossing of the Fetoplacental Barrier by Listeria monocytogenes. Infect. Immun. 75: 950-957 [Abstract] [Full Text]  


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