Summary
This project aims to identify targetable transplacental immune signaling pathways that contribute to fetal brain pathologies during maternal influenza, with the goal of optimizing antenatal therapies to improve maternal and offspring health outcomes.
What they want
The project will investigate how immune signals propagate across the maternal-fetal interface to impact fetal brain development during gestational influenza virus infection. It hypothesizes that gestational influenza causes leukocyte and lymphocyte infiltration into the placenta, enhancing transplacental inflammation sensed by fetal microglia and border-associated macrophages, leading to fetal brain pathologies. The research will define time-dependent phenotypic and functional shifts in immune and non-immune cells at the maternal-fetal interface, determine placental vascular permeability and leukocyte diapedesis rates and their dependence on IL-6 signaling, and assess the response of fetal brain microglia and macrophages to transplacental IL-6 signaling.
Deliverables
- Identification of targetable transplacental immune signaling pathways
- Definition of time-dependent phenotypic and functional shifts in immune and non-immune cells at the maternal-fetal interface during maternal respiratory influenza infection
- Rates of placental vascular permeability and leukocyte diapedesis and their dependence upon IL-6 signaling
- Understanding of how fetal brain microglia and macrophages shift their proliferation, activation, and colonization patterns in response to transplacental IL-6 signaling
- Insights for mitigating fetal neuroinflammation during related viral pandemics
Technical requirements
- cutting-edge spatial transcriptomics
