Patients with inflammatory bowel disease (IBD) have altered intestinal microbial composition, but whether this altered microbiota is a cause or consequence of inflammation is unclear. The importance of the gut microbiota in IBD pathogenesis has been shown in many murine models, since colitis fails to develop in genetically-susceptible mice when re-derived into germ-free environments. Wiskott-Aldrich syndrome protein (WASP)-deficient (Was-/-) mice exhibit immune dysregulation and develop IBD, similar to human patients with mutations in WAS.