A research team in France has unraveled the molecular mechanism that allows the invasive microbial pathogen Listeria monocytogenes to target and cross the placenta from mother to baby. Infection with L. monocytogenes can result in miscarriage and stillbirth.
Led by Marc Lecuit from the Pasteur Institute in Paris, the team used two novel animal models — gerbils and a genetically engineered mouse line — to show that two bacterial invasion proteins, In1A and In1B, are required for L. monocytogenes to target and cross the placental barrier.
“Our study demonstrates the concordance of epidemiological, in vitro, ex vivo and in vivo data and establishes that L. monocytogenes specifically targets the placenta in vivo, if and only if both In1A and In1B pathways are functional,” write the authors in this week’s edition of Nature. They also note that previous studies, which used the mouse and guinea pig as models, “found no role for In1A or In1B in placental invasion.”
According to Lecuit and colleagues, this is the first study that demonstrates species- and tissue-specific recognition of the placenta, which enables it to breach the placental barrier.
This understanding of how the microbe can cross the host’s natural barrier could help in the development of inhibiting molecules for use as preventative therapies.
- Conjugated action of two species-specific invasion proteins for fetoplacental listeriosis (Letter p1114, doi: 10.1038/nature07303)
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