Chronic inflammation is a common denominator in a wide range of diseases originating from various tissues. The epithelial barriers of the skin, lungs, and gut, which protect our body from insults, are constantly at risk of inflammation due to wounds, environmental factors (e.g., microbes, ultraviolet radiation), and genetic predispositions. Inflammatory epithelial conditions have long been postulated to be hyperactive injury responses, co-opting transcriptional programs involved in wound repair to drive epithelial dysfunction. Many aspects of repair that rely on immune or cytokine signals are amplified in inflammatory diseases, including excessive epidermal growth, hypervascularization, hyperinnervation, and immune activation. Our lab is leveraging principles from the wound healing process to uncover novel cellular mechanisms that could serve as therapeutic approaches for inflammatory conditions characterized by damage-repair pathologies.