Creeping fat represents a disease characterizing finding in Crohn’s disease but its impact on intestinal inflammation and epithelial barrier function is unknown. The present project aims to define how intestinal barrier defects shape the homeostasis of mesenteric fat, how these alterations confer to an alternative intestinal barrier and how creeping fat modulates epithelial resistance as well as intestinal immune cell composition and immunity. A fat-depleting mouse model will serve to answer these questions and the data will subsequently be correlated to results obtained from a Crohn’s disease patient cohort.