ArticleBMC genomics2013
Genetic analysis of the Trichuris muris-induced model of colitis reveals QTL overlap and a novel gene cluster for establishing colonic inflammation.
Article in BMC genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens.Nature genetics · 2014Pooled it
- Circadian clock-related genome-wide mendelian randomization identifies putatively genes for ulcerative colitis and its comorbidity.BMC genomics · 2024Article
- Platelet indices and inflammatory bowel disease: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Causal association between inflammatory bowel disease and hidradenitis suppurativa: A two-sample bidirectional Mendelian randomization study.Frontiers in immunology · 2023Article
- Novel long non-coding RNAs of relevance for ulcerative colitis pathogenesis.Non-coding RNA research · 2022Article
- Article
- Differential Expression of Soluble Receptor for Advanced Glycation End-products in Mice Susceptible or Resistant to Chronic Colitis.Inflammatory bowel diseases · 2020Article
- Immunity to gastrointestinal nematode infections.Mucosal immunology · 2018Review
- Self-adjuvanting C18 lipid vinil sulfone-PP2A vaccine: study of the induced immunomodulation againstOpen biology · 2017Article
- The Hygiene Hypothesis and Its Inconvenient Truths about Helminth Infections.PLoS neglected tropical diseases · 2016Article
- New developments in the genetics, pathogenesis, and therapy of IgA nephropathy.Kidney international · 2015Review
- Mucosal immune responses following intestinal nematode infection.Parasite immunology · 2014Review
- Whipworm genome and dual-species transcriptome analyses provide molecular insights into an intimate host-parasite interaction.Nature genetics · 2014Article
- 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
- Sex-dependent genetic effects on immune responses to a parasitic nematode.BMC genomics · 2014Article
- The role of mouse strain differences in the susceptibility to fibrosis: a systematic review.Fibrogenesis & tissue repair · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGenetic susceptibility to colonic inflammation is poorly defined at the gene level. Although Genome Wide Association studies (GWAS) have identified loci in the human genome which confer susceptibility to Inflammatory Bowel Disease (Crohn's and Ulcerative Colitis), it is not clear if precise loci exist which confer susceptibility to inflammation at specific locations within the gut e.g. small versus large intestine. Susceptibility loci for colitis in particular have been defined in the mouse, although specific candidate genes have not been identified to date. We have previously shown that infection with Trichuris muris (T. muris) induces chronic colitis in susceptible mouse strains with clinical, histological, and immunological homology to human colonic Crohn's disease. We performed an integrative analysis of colitis susceptibility, using an F2 inter-cross of resistant (BALB/c) and susceptible (AKR) mice following T. muris infection. Quantitative Trait Loci (QTL), polymorphic and expression data were analysed alongside in silico workflow analyses to discover novel candidate genes central to the development and biology of chronic colitis.
results7 autosomal QTL regions were associated with the establishment of chronic colitis following infection. 144 QTL genes had parental strain SNPs and significant gene expression changes in chronic colitis (expression fold-change ≥ +/-1.4). The T. muris QTL on chromosome 3 (Tm3) mapped to published QTL in 3 unrelated experimental models of colitis and contained 33 significantly transcribed polymorphic genes. Phenotypic pathway analysis, text mining and time-course qPCR replication highlighted several potential cis-QTL candidate genes in colitis susceptibility, including FcgR1, Ptpn22, RORc, and Vav3.
conclusionGenetic susceptibility to induced colonic mucosal inflammation in the mouse is conserved at Tm3 and overlays Cdcs1.1. Genes central to the maintenance of intestinal homeostasis reside within this locus, implicating several candidates in susceptibility to colonic inflammation. Combined methodology incorporating genetic, transcriptional and pathway data allowed identification of biologically relevant candidate genes, with Vav3 newly implicated as a colitis susceptibility gene of functional relevance.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.