Placental Syncytiotrophoblast Constitutes a Major Barrier to Vertical Transmission of Listeria monocytogenes

PLoS Pathogens

Varvara B. Zeldovich¹  Jennifer R. Robbins²  Mirhan Kapidzic²  Anna I. Bakardjiev³  Kasia M. Skrzypczynska³ 

[1] Department of Biology, Xavier University, Cincinnati, Ohio, United States of America;Department of Pediatrics, University of California, San Francisco, California, United States of America;Program in Microbial Pathogenesis and Host Defense, University of California, San Francisco, California, United States of America

关键词: Listeria monocytogenes;    Placenta;    Intracellular pathogens;    Blood;    Decidua;    Pregnancy;    Histology;    Pathogens;   

DOI  :  10.1371/journal.ppat.1000732

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

Listeria monocytogenes is an important cause of maternal-fetal infections and serves as a model organism to study these important but poorly understood events. L. monocytogenes can infect non-phagocytic cells by two means: direct invasion and cell-to-cell spread. The relative contribution of each method to placental infection is controversial, as is the anatomical site of invasion. Here, we report for the first time the use of first trimester placental organ cultures to quantitatively analyze L. monocytogenes infection of the human placenta. Contrary to previous reports, we found that the syncytiotrophoblast, which constitutes most of the placental surface and is bathed in maternal blood, was highly resistant to L. monocytogenes infection by either internalin-mediated invasion or cell-to-cell spread. Instead, extravillous cytotrophoblasts—which anchor the placenta in the decidua (uterine lining) and abundantly express E-cadherin—served as the primary portal of entry for L. monocytogenes from both extracellular and intracellular compartments. Subsequent bacterial dissemination to the villous stroma, where fetal capillaries are found, was hampered by further cellular and histological barriers. Our study suggests the placenta has evolved multiple mechanisms to resist pathogen infection, especially from maternal blood. These findings provide a novel explanation why almost all placental pathogens have intracellular life cycles: they may need maternal cells to reach the decidua and infect the placenta.

【 授权许可】

CC BY