ArticleInflammatory bowel diseases2010
Cdcs1 a major colitis susceptibility locus in mice; subcongenic analysis reveals genetic complexity.
Article in Inflammatory bowel diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- The IL-10 receptor inhibits cell extrinsic signals necessary for STAT1-dependent macrophage accumulation during colitis.Mucosal immunology · 2023Article
- IL-10 Receptor Neutralization-Induced Colitis in Mice: A Comprehensive Guide.Current protocols · 2021Article
- ADP-heptose: a bacterial PAMP detected by the host sensor ALPK1.Cellular and molecular life sciences : CMLS · 2021Review
- Citrobacter rodentium induces rapid and unique metabolic and inflammatory responses in mice suffering from severe disease.Cellular microbiology · 2020Article
- Temporal Dynamics of Chronic Inflammation on the Cecal Microbiota in IL-10Frontiers in immunology · 2020Article
- CD14 and ALPK1 Affect Expression of Tight Junction Components and Proinflammatory Mediators upon Bacterial Stimulation in a Colonic 3D Organoid Model.Stem cells international · 2020Article
- Analysis of Cdcs1 colitogenic effects in the hematopoietic compartment reveals distinct microbiome interaction and a new subcongenic interval active in T cells.Mucosal immunology · 2019Article
- Coordination of Immune-Stroma Crosstalk by IL-6 Family Cytokines.Frontiers in immunology · 2019Review
- Alpha kinase 1 controls intestinal inflammation by suppressing the IL-12/Th1 axis.Nature communications · 2018Article
- Macrophage dysfunction initiates colitis during weaning of infant mice lacking the interleukin-10 receptor.eLife · 2017Article
- Transcription Factor SP2 Enhanced the Expression of Cd14 in Colitis-Susceptible C3H/HeJBir.PloS one · 2016Article
- A Multihit Model: Colitis Lessons from the Interleukin-10-deficient Mouse.Inflammatory bowel diseases · 2015Review
- Immune diseases caused by mutations in kinases and components of the ubiquitin system.Nature immunology · 2014Review
- 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
- Genetic analysis of the Trichuris muris-induced model of colitis reveals QTL overlap and a novel gene cluster for establishing colonic inflammation.BMC genomics · 2013Article
- Identification of a genetic locus controlling bacteria-driven colitis and associated cancer through effects on innate inflammation.The Journal of experimental medicine · 2012Article
- Strain-specific modifier genes governing craniofacial phenotypes.Birth defects research. Part A, Clinical and molecular teratology · 2012Article
- Quantitative trait loci in a bacterially induced model of inflammatory bowel disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Article
- Colitis locus on chromosome 2 impacting the severity of early-onset disease in mice deficient in GPX1 and GPX2.Inflammatory bowel diseases · 2011Article
- Severity of innate immune-mediated colitis is controlled by the cytokine deficiency-induced colitis susceptibility-1 (Cdcs1) locus.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
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11 authors.
Funding
Abstract
backgroundThe cytokine-deficiency-induced colitis susceptibility (Cdcs)1 locus is a major modifier of murine inflammatory bowel disease (IBD) and was originally identified in experimental crosses of interleukin-10-deficient (Il10(-/-)) mice. Congenic mice, in which this locus was reciprocally transferred between IBD-susceptible C3H/HeJBir-Il10(-/-) and resistant C57BL/6J-Il10(-/-) mice, revealed that this locus likely acts by inducing innate hypo- and adaptive hyperresponsiveness, associated with impaired NF-kappaB responses of macrophages. The aim of the present study was to dissect the complexity of Cdcs1 by further development and characterization of reciprocal Cdcs1 congenic strains and to identify potential candidate genes in the congenic interval.
methodsIn total, 15 reciprocal congenic strains were generated from Il10(-/-) mice of either C3H/HeJBir or C57BL/6J genetic backgrounds by 10 cycles of backcrossing. Colitis activity was monitored by histological grading. Candidate genes were identified by fine mapping of congenic intervals, sequencing, microarray analysis, and a high-throughput real-time reverse-transcription polymerase chain reaction (RT-PCR) approach using bone marrow-derived macrophages.
resultsWithin the originally identified Cdcs1-interval, 3 independent regions were detected that likely contain susceptibility-determining genetic factors (Cdcs1.1, Cdcs1.2, and Cdcs1.3). Combining results of candidate gene approaches revealed Fcgr1, Cnn3, Larp7, and Alpk1 as highly attractive candidate genes with polymorphisms in coding or regulatory regions and expression differences between susceptible and resistant mouse strains.
conclusionsSubcongenic analysis of the major susceptibility locus Cdcs1 on mouse chromosome 3 revealed a complex genetic structure. Candidate gene approaches revealed attractive genes within the identified regions.
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