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Infection and Immunity, February 2007, p. 950-957, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01570-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

ActA Is Required for Crossing of the Fetoplacental Barrier by Listeria monocytogenes{triangledown}

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

U-570 INSERM,1 University and Medical School Paris-Descartes,2 Assistance Publique—Hôpitaux de Paris, 75730 Paris Cedex 15, France,3 Département d'Anatomie Pathologique, Hôpital Necker-Enfants Malades, 75015 Paris, France4

Received 28 September 2006/ Returned for modification 17 October 2006/ Accepted 13 November 2006

The facultative intracellular bacterial pathogen Listeria monocytogenes induces severe fetal infection during pregnancy. Little is known about the molecular mechanisms allowing the maternofetal transmission of bacteria. In this work, we studied fetoplacental invasion by infecting mice with various mutants lacking virulence factors involved in the intracellular life cycle of L. monocytogenes. We found that the placenta was highly susceptible to bacteria, including avirulent bacteria, such as an L. monocytogenes mutant with an hly deletion ({Delta}LLO) and a nonpathogenic species, Listeria innocua, suggesting that permissive trophoblastic cells, trapping bacteria, provide a protective niche for bacterial survival. The {Delta}LLO mutant, which is unable to escape the phagosomal compartment of infected cells, failed to grow in the trophoblast tissue and to invade the fetus. Mutant bacteria with inlA and inlB deletion ({Delta}InlAB) grew in the placenta and fetus as well as did the wild-type virulent stain (EGDwt), indicating that in the murine model, internalins A and B are not involved in fetoplacental invasion by L. monocytogenes. Pregnant mice were then infected with an actA deletion ({Delta}ActA) strain, a virulence-attenuated mutant that is unable to polymerize actin and to spread from cell to cell. With the {Delta}ActA mutant, fetal infection occurs, but with a significant delay and restriction, and it requires a placental bacterial load 2 log units higher than that for the wild-type virulent strain. Definitive evidence for the role of ActA was provided by showing that a actA-complemented {Delta}ActA mutant was restored in its capacity to invade fetuses. ActA-mediated cell-to-cell spreading plays a major role in the vertical transmission of L. monocytogenes to the fetus in the murine model.

* Corresponding author. Mailing address: Department of Microbiology-INSERM, 156 rue de Vaugirard, 75730 Paris Cedex 15, France. Phone: 33 1 44 49 49 61. Fax: 33 1 44 49 49 60. E-mail: kayal{at}necker.fr.

{triangledown} Published ahead of print on 21 November 2006.

Editor: D. L. Burns

Infection and Immunity, February 2007, p. 950-957, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01570-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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