Our research interests
We study the pathways by which microorganisms cross cellular barriers and the mechanisms by which these barriers restrict microbial infections. Our research focuses primarily on the epithelial lining of the gastrointestinal tract and placental trophoblasts, the key cellular barrier in the placenta. This multidisciplinary work combines cell biology, immunology, and microbiology to uncover both pathogen- and host-specific therapeutic targets. Ultimately, our goal is to develop preventative and therapeutic strategies that reduce the morbidity and mortality associated with microbial infections.
Exploring the Maternal-Fetal Interface across evolution using Organoids
By leveraging organoid models, we hope to explore the maternal-fetal interface across evolutionary timelines, uncovering unique adaptations that support pregnancy in different mammalian species. These advanced models offer a window into the cellular and molecular interactions that have evolved to nurture and protect developing life.
Antimicrobial Signaling at the Maternal-Fetal Interface
We are interested in defining the mechanisms by which the placenta restricts microbial access to the intrauterine compartment and how teratogenic pathogens including Toxoplasma gondii, CMV, Listeria monocytogenes, Group B strep, and Zika virus bypass these defenses. For these studies, we utilize primary cells and organoids.
Enterovirus Infections at Secondary Tissue Sites
We are interested in identifying receptors for enteroviruses and defining the role of these receptors in pathogenesis. Recently, we identified the neonatal Fc receptor (FcRn) as a primary receptor for echoviruses. Current studies in the lab are focused on using human stem cell-derived enteroids and in vivo mouse models to define the role of FcRn in echovirus pathogenesis in the liver and brain, two sites commonly associated with echovirus-induced disease.
Enterovirus Infections in the gastrointestinal tract
We are interested in defining the mechanisms by which enteroviruses enter and replicate in the GI tract and how this tissue responds to these infections. For these studies, we utilize human and mouse stem cell-derived enteroids and in vivo mouse models and focus on clinically relevant enteroviruses including coxsackievirus B (CVB), echoviruses, enterovirus 71 (EV71), and enterovirus D-68 (EV-D68).