ArticleInflammatory bowel diseases2011
Colitis locus on chromosome 2 impacting the severity of early-onset disease in mice deficient in GPX1 and GPX2.
Article in Inflammatory bowel diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Exposure to air pollution increases susceptibility to ulcerative colitis through epigenetic alterations in CXCR2 and MHC class III region.EBioMedicine · 2024Article
- Exploring the potential function of trace elements in human health: a therapeutic perspective.Molecular and cellular biochemistry · 2023Review
- The beginning of GPX2 and 30 years later.Free radical biology & medicine · 2022Review
- Single-cell analyses of Crohn's disease tissues reveal intestinal intraepithelial T cells heterogeneity and altered subset distributions.Nature communications · 2021Article
- Organic Selenium Increased Gilts Antioxidant Capacity, Immune Function, and Changed Intestinal Microbiota.Frontiers in microbiology · 2021Article
- Role of the microbiota in ileitis of a mouse model of inflammatory bowel disease-Glutathione peroxide isoenzymes 1 and 2-double knockout mice on a C57BL background.MicrobiologyOpen · 2020Article
- Micronutrient Absorption and Related Outcomes in People with Inflammatory Bowel Disease: A Review.Nutrients · 2019Review
- Expression of inositol-requiring enzyme 1β is downregulated in azoxymethane/dextran sulfate sodium-induced mouse colonic tumors.Experimental and therapeutic medicine · 2019Article
- New Insights into the Role of Trace Elements in IBD.BioMed research international · 2018Review
- Deficiency in Duox2 activity alleviates ileitis in GPx1- and GPx2-knockout mice without affecting apoptosis incidence in the crypt epithelium.Redox biology · 2017Article
- Colitis-associated colon cancer: Is it in your genes?World journal of gastroenterology · 2015Review
- Selenium and inflammatory bowel disease.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- The Collaborative Cross as a resource for modeling human disease: CC011/Unc, a new mouse model for spontaneous colitis.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Article
- Nox1 causes ileocolitis in mice deficient in glutathione peroxidase-1 and -2.Free radical biology & medicine · 2014Article
- The Gdac1 locus modifies spontaneous and Salmonella-induced colitis in mice deficient in either Gpx2 or Gpx1 gene.Free radical biology & medicine · 2013Article
- Expression of lactoperoxidase in differentiated mouse colon epithelial cells.Free radical biology & medicine · 2012Article
- Analysis of candidate colitis genes in the Gdac1 locus of mice deficient in glutathione peroxidase-1 and -2.PloS one · 2012Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGenetic background has a profound effect on inflammatory bowel disease. The Gpx1 and Gpx2 double knockout (GPX1/2-DKO) mice on a mixed C57BL/6 (B6) and 129S1/SvimJ (129) background exhibit spontaneous ileocolitis. The DKO mice on a B6 background have mild ileocolitis. We characterized the 129 DKO mice to identify a genetic locus affecting disease severity.
methodsWe backcrossed B6;129 DKO mice to 129 and analyzed for ileocolitis penetrance and severity at N5, N7, and N10. By correlating disease severity with single-nucleotide polymorphism (SNP) markers, we identified a colitis locus.
resultsAs early as 9 days of age, 129 DKO N5 and N10 mice showed disease signs and morbidity. The N10 DKO mice had the severest colitis with nearly complete penetrance and high morbidity compared with other generations or backgrounds. 129 DKO mice had elevated colonic KC and SAA3 expression, shorter colon length, and cecal E. coli overgrowth compared to B6 DKO mice. Analysis of the B6 loci in 129 N5, N7, and N10 cohorts pointed to a region of chromosome 2: 119 Mbp contributing to mild symptoms.
conclusionsGPX1/2-DKO mice on 129 genetic background have the most aggressive colitis compared to B6;129 and B6 colonies. A B6 locus significantly contributing the resistance resides on chromosome 2: 119 Mbp. This region coincides with cytokine-deficiency-induced colitis susceptibility, Cdcs3, identified in the resistant B6 and sensitive C3H/HeJBir (C3Bir) with IL-10 deficiency. A three-way SNP analysis between 129, B6, and C3Bir locus points the major candidate genes to B2m, Dnajc17, Duox2, Pla2g4b, Pla2g4e, Pla2g4f and Slc30a4.
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