Objective: Intestinal Inflammatory Disease (IID) as a primary immunodeficiency depends on mutations in the NADPH oxidase complex, responsible for the production ofreactive oxygen species (ROS). One of the most common clinical patterns in IID is chronic colitis. Ncf1-mutation in mice leads to deficiency in ROS, rendering them susceptible to autoimmunity. Here we studies how ROS-deficiency in Ncf1-mutant mice influenced the immune response to DSS colitis, its recovery and answer to a second induction. Method: Colitis was induced in wild type (WT) and Ncf1mutant (Ncf1) B10.Q mice by administration of 3.5 % DSS in the drinking water for 1 week. After 1 week recovery, DSS was administered for another week. Mice were sacrificed at days 0, 7, 14 and 21, the colon was removed and folded into a Swiss roll. Sections of the colon were stained with HE, and monoclonal antibodies against B cells (B220), CD3+ T cells; and macrophages (Mac1/CD11b) were applied. Results: Colitis was more severe in Ncf1 than WT mice, with epithelial dysplasia, hyperplasia of Peyer's patches and poor epithelium recovery (hyaline scars). At all time-points the amount and location of colonic B cells, T cells and CD11b + cells was distinct between groups. These results suggest that ROS are crucial for leukocyte recruitment and tissue-repair in DSS-induced colitis.