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    Aberrant Epigenetic Regulation Triggers Intestinal Symptoms in Celiac Disease


    Jefferson Adams
    Aberrant Epigenetic Regulation Triggers Intestinal Symptoms in Celiac Disease
    Image Caption: Researchers discover aberrant epigenetic regulation behind the intestinal symptoms in celiac disease. Photo: CC--EveryCarListed P

    Celiac.com 10/11/2016 - Celiac disease is an autoimmune disease in genetically susceptible individuals and is triggered by adverse immune reactions to gluten, a protein found in wheat and other grains.

    Researchers led by a research group at Finland's University of Tampere, led by Keijo Viiri, PhD, recently discovered a mechanism that triggers aberrant features in celiac disease and colorectal cancer. Disturbances in this mechanism seem to trigger certain symptoms celiac disease, and possibly in colorectal cancer.

    The research team's recent study offers new details on the pathogenesis of the differentiation defect of the epithelium in the small intestine in celiac disease. When people with celiac disease eat gluten, they suffer intestinal mucosal damage with villus atrophy and crypt hyperplasia. At the cellular level, epithelial cells are less differentiated and hyper-proliferative leading to the malabsorption of nutrients. Researchers discovered that a certain epigenetic mechanism, called Polycomb, governs the homeostasis between the intestinal stem cells in the crypt and the differentiated epithelium in the villi. Polycomb acts by silencing genes epigenetically by methylating histone proteins that are packing the DNA.

    "Polycomb is well-known for its function to regulate embryonal development. We discovered that Polycomb is also able to regulate the homeostasis of the small intestine in adults. The regulation of intestinal homeostasis is a tremendous task as the epithelium of the intestine needs to be replenished completely every 4-5 days," says Academy of Finland Postdoctoral Researcher and Principal Investigator Keijo Viiri.

    This study demonstrates that in people with celiac disease, dietary gluten triggers excessive activity of Polycomb leading to the aberrant silencing of genes necessary for the differentiation of villus epithelium and to the concomitant differentiation defect in celiac disease. Moreover, the study demonstrates that Polycomb target genes are also dysregulated in colorectal cancer, which suggests that aberrant Polycomb activity is common in intestinal diseases entailing a differentiation defect on the intestinal epithelium.

    From a clinical point of view, this work provides new insight into the pathogenesis of the intestinal damage in celiac disease and provides diagnostic markers for the disease.

    Since Polycomb regulates only genes imperative for development, this work is also instrumental to further understand the biology of the intestinal homeostasis.

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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, and science. He previously served as Health News Examiner for Examiner.com, and provided health and medical content for Sharecare.com.

    Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book Dangerous Grains by James Braly, MD and Ron Hoggan, MA.

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    Jefferson Adams
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    The research team included U Volta, G Caio, E Boschetti, F Giancola, KJ Rhoden, E Ruggeri, P Paterini, and R De Giorgio. They are all affiliated with the Department of Medical and Surgical Sciences, University of Bologna, St. Orsola-Malpighi Hospital, Italy. They looked at clinical, histological and laboratory findings from 810 celiac disease diagnoses, and retrospectively characterized seronegative patients.
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    Jefferson Adams
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    Jefferson Adams
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