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

Listeriosis and other microbial infections in pregnancy can affect the fetus as well as the mother, but little is known about how pathogens cross the placental barrier. Disson et al. investigated the process using two complementary animal models infected by Listeria monocytogenes. They show that two virulence factors or invasion proteins, InlA and InlB, are required for the transfer of pathogen to the placenta. Thus by blocking one or both of these pathways it may be possible to stop microbes passing into the fetus. Conversely, it may be possible to exploit these pathways to target therapeutic molecules across the same barrier. Listeria monocytogenes can cross the placental barrier and may result in fetal or neonatal mortality. Using two complementary animal models, it is now shown that virulence factors InlA and InlB are both required for this process in vivo. 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.