Intestinal fibrosis is a frequent complication in the natural history of inflammatory bowel disease (IBD) as up to one-third of Crohn’s disease (CD) patients, and about 5% of ulcerative colitis (UC) patients develop strictures in the clinical course of the disease. Fibrosis is associated with improper production of extracellular matrix (ECM) components, mainly collagen and fibronectin. Moreover, several cytokines have been shown to exert a pro-fibrogenic action in IBD. This project investigates the mechanism by which transcriptional activity of Nrf2, a key regulator of cellular reduction-oxidation homeostasis and ECM components production, influences colon development and functionality using mice models. We hypothesize that lack of transcriptional activity of Nrf2 contributes to changes in colon morphology by modulating colon fibrosis, oxidative stress, and premature senescence and that Nrf2 may influence colon functionality by changing the expression of tight junction and muscle response to stimulation. Moreover, we suppose that Nrf2 modulates colon development during gestation. As the administration of IL-10 inhibits IBD progression and may be regulated by Nrf2 transcriptional activity, we hypothesize that Nrf2 may lead to increased production of IL-10, which protects healthy mice from IBD.