Research

Our body’s epithelial barriers, such as the skin, lungs, and gut, interface with the external world and are routinely exposed to injurious, microbial, and carcinogenic stimuli. We study how barrier tissues sense, respond to, and remember these encounters. We have recently shown that the epithelia, and in particular epithelial stem cells, maintain a memory of inflammation. In this context, we examine how tissue adaptation promotes anti-pathogen responses and repair. On the other hand, maladaptations of inflammatory memory underlie recurrent autoimmune disease and cancers. We thus seek to understand the mechanisms controlling the delicate balance between beneficial and deleterious features of inflammatory memory.

We also aim to understand the role of immune cells in tissue repair and regeneration by studying mechanisms of immune-tissue crosstalk following acute damage and in chronic non-healing conditions such as skin ulcers and intestinal fistulae. Here, we take unbiased approaches to track the evolution of immune populations in wounds and then examine their pro- or anti-repair functions. Cancers have long been called “wounds that don’t heal” and so we parallel our studies in acute wounds with an understanding of cancer development and progression.

A veritable garden of commensal bacteria, fungi, and viruses reside in and on our bodies. Far from bystanders, these microbes are essential for maintaining host physiology, providing vital signals to sustain health. Our lab studies how host-commensal interactions train our epithelial barriers. In particular, we are interested in identifying the spatial and functional interactions between commensal microbes and epithelial stem and differentiated cells at steady state and during wounding. Do certain microbial signals stimulate regeneration and others delay it? Can stem cells sense commensals or is this sensing relegated to their differentiated progeny? Do microbial metabolites condition the epithelia? 

Additionally, the invading pathogens that penetrate our boundaries cause tissue damage. The fascinating antagonism between an infection and wound repair is central to the pathology of many diseases, including Staphylococcus aureus infections and chronic non-healing wounds. By untangling the dynamic interactions between host and pathogen, we aim to uncover new ways to combat these conditions.