| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3399188 | Current Opinion in Microbiology | 2012 | 8 Pages |
Placental infections are major causes of maternal and fetal disease. This review introduces a new paradigm for placental infections based on current knowledge of placental defenses and how this barrier can be breached. Transmission of pathogens from mother to fetus can occur at two sites of direct contact between maternal cells and specialized fetal cells (trophoblasts) in the human placenta: firstly, maternal immune and endothelial cells juxtaposed to extravillous trophoblasts in the uterine implantation site and secondly, maternal blood surrounding the syncytiotrophoblast (SYN). Recent findings suggest that the primary vulnerability is in the implantation site. We explore evidence that the placental SYN evolved as a defense against pathogens, and that inflammation-mediated spontaneous abortion may benefit mother and pathogen.
► The placenta presents multiple defenses against pathogens. ► The syncytiotrophoblast lacks intercellular junctions that contribute to pathogen resistance. ► The uterine-trophoblast environment is rich in innate cellular defenses. ► The few pathogens that can circumvent these barriers have intracellular life cycles.
