Our research group studies basic mechanisms leading to infection of the placenta and vertical transmission of pathogens. As a model pathogen, we use Listeria monocytogenes , a Gram-positive bacterium that can invade and grow within the cytosol of many cell types. L. monocytogenes is a common contaminant of processed foods and, when ingested by a pregnant woman, can infect placental tissues and the fetus. Depending on the gestational age L. monocytogenes infection during pregnancy can lead to spontaneous abortion, preterm labor, or neonatal disease with very high morbidity and mortality.

We have developed a novel pregnant guinea pig model of listeriosis that replicates human disease, as the placental architecture of guinea pigs closely resembles humans. The placenta is a chimeric structure derived from maternal and fetal components. Fetally derived cells called trophoblasts form a tight physical barrier between maternal and fetal circulation, and we have shown that L. monocytogenes can be found in the trophoblasts of intravenously infected guinea pigs. Subsequently L. monocytogenes spreads from the placenta to fetal tissues.

We are now exploiting the pregnant guinea pig model to understand how L. monocytogenes disseminates from the intestine to the placenta, and which listerial virulence factors are involved in this process. In addition, we are characterizing L. monocytogenes infection of primary human trophoblasts and placental explants to dissect the molecular and cellular mechanisms of trophoblast infection as well as the placental response. Together, these studies will allow us to dissect the pathways by which pathogens cross the trophoblast layer in vivo and characterize the role of trophoblasts in the defense against infection.