Defining Interactions Between the Genome, Epigenome, and the Environment in Inflammatory Bowel Disease: Progress and Prospects Gastroenterology. 2023 Apr 14;S0016-5085(23)00619-4.doi: 10.1053/j.gastro.2023.03.238. Online ahead of print.
Alexandra J Noble 1, Jan K Nowak 2, Alex T Adams 3, Holm H Uhlig 4, Jack Satsangi 3 |
Author information 1Translational Gastroenterology Unit, Nuffield Department of Experimental Medicine, University of Oxford, Oxford, United Kingdom. Electronic address: Alexandra.noble@ndm.ox.ac.uk. 2Department of Paediatric Gastroenterology and Metabolic Diseases, Poznan University of Medical Sciences, Poznan, Poland. 3Translational Gastroenterology Unit, Nuffield Department of Experimental Medicine, University of Oxford, Oxford, United Kingdom. 4Translational Gastroenterology Unit, Nuffield Department of Experimental Medicine, University of Oxford, Oxford, United Kingdom; Department of Paediatrics, University of Oxford, Oxford, United Kingdom; Biomedical Research Centre, University of Oxford, Oxford, United Kingdom. Abstract Recent advances in our understanding of the pathogenesis of inflammatory bowel disease (IBD) have highlighted the complex interplay between the genome, the epigenome, and the environment. Despite the exciting advances in genomics that have enabled the identification of over 200 susceptibility loci, these only account for a small proportion of the disease variance and the estimated heritability in IBD. It is likely that gene-environment (GxE) interactions contribute to "missing heritability" and these may act through epigenetic mechanisms. Several environmental factors, such as the microbiome, nutrition, and tobacco smoking, induce alterations in the epigenome of children and adults, which may impact disease susceptibility. Other mechanisms for GxE interactions are also directly pertinent in early life. We discuss a model in which environmental factors imprint disease risk in a window of susceptibility during infancy that may contribute to later disease onset, whereas other elements of the exposome act later in life and contribute directly to the pathogenesis and course of the disease. Understanding the mechanisms underlying GxE interactions may provide the basis for new therapeutic targets or preventative strategies for IBD.
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