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Background  The  Mutyh  DNA glycosylase is involved in the repair of oxidized DNA bases. Mutations in the human  MUTYH  gene are responsible for colorectal cancer in familial adenomatous polyposis. Since defective DNA repair genes might contribute to the increased cancer risk associated with inflammatory bowel diseases, we compared the inflammatory response of wild-type and  Mutyh −/−   mice to oxidative stress.    Methodology/Principal Findings  The severity of colitis, changes in expression of genes involved in DNA repair and inflammation, DNA 8-oxoguanine levels and microsatellite instability were analysed in colon of mice treated with dextran sulfate sodium (DSS). The  Mutyh −/−   phenotpe was associated with a significant accumulation of 8-oxoguanine in colon DNA of treated mice. A single DSS cycle induced severe acute ulcerative colitis in wild-type mice, whereas lesions were modest in  Mutyh −/−   mice, and this was associated with moderate variations in the expression of several cytokines. Eight DSS cycles caused chronic colitis in both wild-type and  Mutyh −/−   mice. Lymphoid hyperplasia and a significant reduction in Foxp3 +  regulatory T cells were observed only in  Mutyh −/−   mice.    Conclusions  The findings indicate that, in this model of ulcerative colitis, Mutyh plays a major role in maintaining intestinal integrity by affecting the inflammatory response.

The Mutyh Base Excision Repair Gene Influences the Inflammatory Response in a Mouse Model of Ulcerative Colitis