ArticleInternational journal of colorectal disease2012
The JAK2 variant rs10758669 in Crohn's disease: altering the intestinal barrier as one mechanism of action.
Article in International journal of colorectal disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.
- JAK2 rs10758669 polymorphisms and susceptibility to ulcerative colitis and Crohn's disease: a meta-analysis.Inflammation · 2014Pooled it
- Pooled it
- Intestinal epithelial cell-specific deletion of Jak2 disrupts gut homeostasis.Scientific reports · 2026Article
- Research progress on the use of polyphenols in the treatment of Crohn's disease.Frontiers in pharmacology · 2025Review
- Exploring inflammatory bowel disease therapy targets through druggability genes: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Article
- The Role of Genetic Factors in the Development of Acute Respiratory Viral Infection COVID-19: Predicting Severe Course and Outcomes.Biomedicines · 2022Article
- Arbutin Ameliorates Murine Colitis by Inhibiting JAK2 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Vitamin D Modulates Intestinal Microbiota in Inflammatory Bowel Diseases.International journal of molecular sciences · 2020Review
- Differential regulation of JAK/STAT-signaling in patients with ulcerative colitis and Crohn's disease.World journal of gastroenterology · 2020Review
- Innate Lymphoid Cells in Crohn's Disease.Frontiers in immunology · 2020Review
- Protein Tyrosine Phosphatases: Regulators of CD4 T Cells in Inflammatory Bowel Disease.Frontiers in immunology · 2018Review
- Inflammatory Bowel Disease: Updates on Molecular Targets for Biologics.Gut and liver · 2017Review
- JAK2 Disease-Risk Variants Are Gain of Function and JAK Signaling Threshold Determines Innate Receptor-Induced Proinflammatory Cytokine Secretion in Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Investigation of JAKs/STAT-3 in lipopolysaccharide-induced intestinal epithelial cells.Clinical and experimental immunology · 2016Article
- Genetic Influences on the Development of Fibrosis in Crohn's Disease.Frontiers in medicine · 2016Review
- Immunopathogenesis of IBD: current state of the art.Nature reviews. Gastroenterology & hepatology · 2016Review
- Genetic effects of single nucleotide polymorphisms in JAK2 and STAT5A genes on susceptibility of Chinese Holsteins to mastitis.Molecular biology reports · 2014Article
- Immunology of inflammatory bowel disease and molecular targets for biologics.Gastroenterology clinics of North America · 2014Review
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe aetiology of intestinal barrier dysfunction in Crohn's disease (CD) is poorly understood. Associations in relatives of CD families suggest a genetic basis, but the relevant variants are still unknown. We hypothesized that variants in genes occurring in pathways such as autophagy and IL23 signalling might contribute to CD by altering intestinal permeability.
methodsWe analysed five variants (rs10758669 within JAK2, rs744166 within STAT3, rs4958847, rs11747270 and rs13361189 within IRGM) in adult German inflammatory bowel disease patients (CD, n = 464; ulcerative colitis (UC), n = 292) and matched healthy controls (n = 508). These data were correlated with gastrointestinal permeability as assessed by lactulose/mannitol ratio in CD patients (n = 141) in remission.
resultsOur data confirm the association between JAK2 rs10758669 (p = 0.026, OR = 1.25, 95% CI = 1.04-1.50) and STAT3 rs744166 (p = 0.04, OR = 0.83, 95% CI = 0.688-0.998) with CD, but not UC. With respect to all the analysed IRGM variants, no association was found to either CD or UC. Among CD patients, an increased intestinal permeability was detected in 65 out of 141 patients (46.1%). Most importantly, patients carrying the C risk allele within JAK2 rs10758669 displayed an increased permeability more often compared with patients without the C allele (p = 0.004). No association with intestinal permeability was found for STAT3 rs744166 and all IRGM variants.
conclusionsJAK2 rs10758669 and STAT3 rs744166 increase susceptibility for CD. We show that the A>C substitution in rs10758669 of the JAK2 gene is associated with increased intestinal permeability. Altering intestinal barrier function might thus be one mechanism how JAK2 contributes to CD pathogenesis.
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