File:Listeria maternal-fetal barrier.jpg

Model of L. monocytogenes mechanisms for breaching the maternal-fetal barrier.

L. monocytogenes is subjected to multiple bottlenecks when infecting the placenta. Our data support extravillous cytotrophoblasts (EVT) as the primary portal of entry. First (1), relatively few L. monocytogenes reach the maternal decidua, carried by phagocytes. These can infect extravillous cytotrophoblasts by cell-to-cell spread, or by lysing the leukocyte and subsequently infecting extravillous cytotrophoblasts via InlA-E-cadherin interactions. (2) Extravillous cytotrophoblasts further winnow bacterial numbers by delaying the L. monocytogenes intracellular life cycle. If infection progresses, bacteria spread through subsyncytial cytotrophoblasts. (3) The basement membrane underlying these cells presents a third barrier, which few bacteria cross to invade the fetal stroma (STR). On the other hand, L. monocytogenes in the blood contacts only the syncytiotrophoblast (SYN), which is highly resistant to both internalin-mediated infection and intercellular spread. However, it is possible that sites of syncytial damage provide access to subsyncytial cytotrophoblasts. In vivo, such sites are rapidly covered by fibrinoid clots [28] that may present yet another physical barrier to infection.