Inflammatory Bowel Disease (IBD) damages the intestine through two connected problems: inflammation (swelling) and fibrosis (scarring). Emerging research reveals that fibroblasts—the cells responsible for scarring—also actively drive inflammation. Unfortunately, no current therapy effectively treats both.
Our project unites a pediatric gastroenterologist and a pediatric surgeon to tackle this challenge. We focus on IL13Rα2, a protein found on intestinal fibroblasts. While previously considered to have a limited role in how cells behave, our data suggests this protein acts as a harmful “switch” that triggers fibroblasts to worsen both inflammation and scarring.
To prove this, we will use a groundbreaking animal model that mimics the thick, fatty scarring seen in Crohn’s disease, along with specialized mice engineered to genetically delete this protein specifically in fibroblasts. We will study how IL13Rα2 drives inflammation and scar tissue formation at the cellular level. Simultaneously, we will test whether removing this protein prevents the intestine from becoming inflamed and stiff. If successful, this work will validate a new biological target, laying the essential groundwork for therapies that prevent intestinal damage and reduce the need for surgery.
