University of Florida in 2002 and graduated with a PhD from The Pennsylvania State University in 2009, majoring in Animal Science with a focus on Reproductive Biology and Immunology. Afterwards, she completed post-doctoral training in the Department of Obstetrics, Gynecology and Reproductive Sciences at the Yale School of Medicine, primarily working with murine models of polymicrobial infections during pregnancy. She is currently an Assistant Professor in the Department of Obstetrics, Gynecology and Reproductive Biology within the College of Human Medicine at Michigan State University.
The main objective(s) of the Racicot Lab are:
- Understanding how maternal stress during pregnancy affects fetal immune development, and how that relates to development of allergic asthma in future offspring. Maternal stress induces changes in the placenta and is associated with allergic asthma development in the future offspring. Our studies address the role of placental dysregulation in fetal programming and development of diseases such as allergic asthma.
- Characterizing the role of placental microflora in fetal immune development. While historically the upper reproductive tract was thought to be a sterile environment during pregnancy, there is now evidence the healthy placenta is home to a vibrant microflora. We hypothesize the fetal environment is influenced by both the presence of these microflora and the placental/maternal response that they elicit, and they contribute to the development and maturation of the fetal immune system.
- Determining how maternal and/or placental viral infection affects fetal brain development in the absence of congenital infection. Viral transmission to the fetus, in utero, can result in devastating neurodevelopmental outcomes including hearing/vision loss, cerebral palsy, and potentially, autism spectrum disorders. Fortunately, viral transmission is extremely rare because viruses typically cannot pass the placenta. Despite this, viruses can infect the placenta and these infections can significantly change placental signaling and function. We hypothesize that the placental response to virus can also affect fetal brain development, even in the absence of viral transmission to the fetus.