The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cells

Abnormal DNA methylation has been described in human inflammatory conditions of the gastrointestinal tract, such as inflammatory bowel disease (IBD). As other complex diseases, IBD results from the balance between genetic predisposition and environmental exposures. As such, DNA methylation may be th...

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Main Authors: Iolanda Agliata, Nora Fernandez-Jimenez, Chloe Goldsmith, Julien C. Marie, Jose R. Bilbao, Robert Dante, Hector Hernandez-Vargas
Format: Article
Language:English
Published: Taylor & Francis Group 2020-10-01
Series:Epigenetics
Subjects:
Online Access:http://dx.doi.org/10.1080/15592294.2020.1748916
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author Iolanda Agliata
Nora Fernandez-Jimenez
Chloe Goldsmith
Julien C. Marie
Jose R. Bilbao
Robert Dante
Hector Hernandez-Vargas
author_facet Iolanda Agliata
Nora Fernandez-Jimenez
Chloe Goldsmith
Julien C. Marie
Jose R. Bilbao
Robert Dante
Hector Hernandez-Vargas
author_sort Iolanda Agliata
collection DOAJ
description Abnormal DNA methylation has been described in human inflammatory conditions of the gastrointestinal tract, such as inflammatory bowel disease (IBD). As other complex diseases, IBD results from the balance between genetic predisposition and environmental exposures. As such, DNA methylation may be the consequence (and potential effector) of both, genetic susceptibility variants and/or environmental signals such as cytokine exposure. We attempted to discern between these two non-excluding possibilities by performing a combined analysis of published DNA methylation data in intestinal mucosal cells of IBD and control samples. We identified abnormal DNA methylation at different levels: deviation from mean methylation signals at site and region levels, and differential variability. A fraction of such changes is associated with genetic polymorphisms linked to IBD susceptibility. In addition, by comparing with another intestinal inflammatory condition (i.e., coeliac disease) we propose that aberrant DNA methylation can also be the result of unspecific processes such as chronic inflammation. Our characterization suggests that IBD methylomes combine intrinsic and extrinsic responses in intestinal mucosal cells, and could point to knowledge-based biomarkers of IBD detection and progression.
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spelling doaj.art-c9b582c2535140b0b62ca178a3d451772023-09-21T13:09:23ZengTaylor & Francis GroupEpigenetics1559-22941559-23082020-10-0115101068108210.1080/15592294.2020.17489161748916The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cellsIolanda Agliata0Nora Fernandez-Jimenez1Chloe Goldsmith2Julien C. Marie3Jose R. Bilbao4Robert Dante5Hector Hernandez-Vargas6University of MoliseUniversity of the Basque Country (UPV/EHU) and Biocruces-Bizkaia Health Research InstituteCancer Research Centre of Lyon (CRCL), Inserm U 1052, CNRS UMR 5286, Université de Lyon, Centre Léon BérardCancer Research Centre of Lyon (CRCL), Inserm U 1052, CNRS UMR 5286, Université de Lyon, Centre Léon BérardUniversity of the Basque Country (UPV/EHU) and Biocruces-Bizkaia Health Research InstituteUniversité de LyonCancer Research Centre of Lyon (CRCL), Inserm U 1052, CNRS UMR 5286, Université de Lyon, Centre Léon BérardAbnormal DNA methylation has been described in human inflammatory conditions of the gastrointestinal tract, such as inflammatory bowel disease (IBD). As other complex diseases, IBD results from the balance between genetic predisposition and environmental exposures. As such, DNA methylation may be the consequence (and potential effector) of both, genetic susceptibility variants and/or environmental signals such as cytokine exposure. We attempted to discern between these two non-excluding possibilities by performing a combined analysis of published DNA methylation data in intestinal mucosal cells of IBD and control samples. We identified abnormal DNA methylation at different levels: deviation from mean methylation signals at site and region levels, and differential variability. A fraction of such changes is associated with genetic polymorphisms linked to IBD susceptibility. In addition, by comparing with another intestinal inflammatory condition (i.e., coeliac disease) we propose that aberrant DNA methylation can also be the result of unspecific processes such as chronic inflammation. Our characterization suggests that IBD methylomes combine intrinsic and extrinsic responses in intestinal mucosal cells, and could point to knowledge-based biomarkers of IBD detection and progression.http://dx.doi.org/10.1080/15592294.2020.1748916dna methylationinflammatory bowel disease (ibd)biomarkerscoeliac disease (ced)methylation quantitative trait loci (mqtls)
spellingShingle Iolanda Agliata
Nora Fernandez-Jimenez
Chloe Goldsmith
Julien C. Marie
Jose R. Bilbao
Robert Dante
Hector Hernandez-Vargas
The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cells
Epigenetics
dna methylation
inflammatory bowel disease (ibd)
biomarkers
coeliac disease (ced)
methylation quantitative trait loci (mqtls)
title The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cells
title_full The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cells
title_fullStr The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cells
title_full_unstemmed The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cells
title_short The DNA methylome of inflammatory bowel disease (IBD) reflects intrinsic and extrinsic factors in intestinal mucosal cells
title_sort dna methylome of inflammatory bowel disease ibd reflects intrinsic and extrinsic factors in intestinal mucosal cells
topic dna methylation
inflammatory bowel disease (ibd)
biomarkers
coeliac disease (ced)
methylation quantitative trait loci (mqtls)
url http://dx.doi.org/10.1080/15592294.2020.1748916
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