ArticleJournal of gastroenterology2011
Ectopic expression of blood type antigens in inflamed mucosa with higher incidence of FUT2 secretor status in colonic Crohn's disease.
Article in Journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Association of Fucosyltransferase 2 Gene Variant with Inflammatory Bowel Diseases: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019Pooled it
- FUT2-mediated α1,2-fucosylation in inflammatory bowel disease: mechanisms and translational potential.Molecular biology reports · 2026Review
- Fucosylation in digestive inflammatory diseases and cancers: From mechanical studies to clinical translation.Genes & diseases · 2025Review
- Correlation Of Fut2 And Fut3 Gene Polymorphisms With Inflammatory Bowel Disease In Guangxi Zhuang Population.International journal of general medicine · 2025Article
- Changes in the Phenotype and Metabolism of Peritoneal Macrophages in Mucin-2 Knockout Mice and Partial Restoration of Their Functions In Vitro After L-Fucose Treatment.International journal of molecular sciences · 2024Article
- ABO Blood Type and Clinical Characteristics Among Japanese Patients With Ulcerative Colitis.Cureus · 2024Article
- Are Changes in Serum IgG Glycosylation Related to the Severe Course of SARS-CoV-2 Infection and Recovery Process? In Search of New Diagnostic and Prognostic Biomarkers.Journal of inflammation research · 2024Article
- Glycosylation-Engineered Platelet Membrane-Coated Interleukin 10 Nanoparticles for Targeted Inhibition of Vascular Restenosis.International journal of nanomedicine · 2023Article
- Microbiota-induced regulatory T cells associate withFrontiers in microbiology · 2023Article
- Finding the sweet spot: glycosylation mediated regulation of intestinal inflammation.Mucosal immunology · 2022Review
- Fucosyltransferase 2: A Genetic Risk Factor for Intestinal Diseases.Frontiers in microbiology · 2022Review
- The Alterations of Serum IgG Fucosylation as a Potential Additional New Diagnostic Marker in Advanced Endometriosis.Journal of inflammation research · 2022Article
- Inhibition of Aberrant α(1,2)-Fucosylation at Ocular Surface Ameliorates Dry Eye Disease.International journal of molecular sciences · 2021Article
- Enteric Viruses and Inflammatory Bowel Disease.Viruses · 2021Review
- Review
- Human microbiota, blood group antigens, and disease.Wiley interdisciplinary reviews. Systems biology and medicine · 2018Review
- Association of Fucosyltransferase 2 Gene Polymorphisms with Inflammatory Bowel Disease in Patients from Southeast China.Gastroenterology research and practice · 2017Article
- Epithelial glycosylation in gut homeostasis and inflammation.Nature immunology · 2016Review
- IL-10-producing CD4(+) T cells negatively regulate fucosylation of epithelial cells in the gut.Scientific reports · 2015Article
- Intestinal fucose as a mediator of host-microbe symbiosis.Journal of immunology (Baltimore, Md. : 1950) · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHost-intestinal microbial interaction plays an important role in the pathogenesis of inflammatory bowel diseases (IBDs). The surface molecules of the intestinal epithelium act as receptors for bacterial adhesion and regulate the intestinal bacteria. Some known receptors are the mucosal blood type antigens, which are regulated by the fucosyltransferase2 (FUT2) gene, and individuals who express these antigens in the gastrointestinal tract are called secretors. Recent research has revealed that the FUT2 gene is associated with Crohn's disease (CD) in western populations.
methodsTo clarify the contribution of mucosal blood type antigens in IBD, we determined the incidence of five previously reported single-nucleotide polymorphisms of the FUT2 gene in Japanese patients. We also used immunohistochemistry to investigate the antigen expression in mucosal specimens from IBD patients and animal models.
resultsGenetic analysis revealed that all of the patients with colonic CD were secretors, whereas the incidence of secretors was 80, 80, 67, and 80%, respectively, for the control, ileocolonic CD, ileal CD, and ulcerative colitis groups (P = 0.036). Abnormal expression of blood type antigens was observed only in colonic CD. Interleukin-10⁻/⁻ mice, but not dextran sulfate sodium colitis mice, had enhanced colonic expression of blood type antigens, and the expression of these antigens preceded the development of colitis in the interleukin-10⁻/⁻ mice.
conclusionsFUT2 secretor status was associated with colonic-type CD. This finding, taken together with the immunohistochemistry data, suggests that the abnormal expression of blood type antigens in the colon may be a unique and essential factor for colonic CD.
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.