The Role of Epigenetic Mechanism in the Pathogenesis of Inflammatory Bowel Disease

Abstract

Inflammatory bowel disease (IBD) is a chronic inflammation of the intestine due to interaction between inappropriate immune response and environmental factors. It consists of ulcerative colitis and Crohn’s disease. The incidence of IBD is increasing globally and disrupts patient’s quality of life and causes heavy economic burden. Several risk factors are involved in IBD including genetic, environment, lifestyle, and socioeconomic status. Antigen enters host’s gastrointestinal tract and triggers an immune reaction. In subject with IBD, the immune reaction is hyperactive. Some conditions such as intestinal barrier disintegration, gut microorganism imbalance, molecular mimicry, and abnormal autophagy trigger chronic inflammation and end with IBD. Genetic predisposition plays a central role in IBD. NOD2, IL23R, and ATG16L1 have the most significant association with IBD. With the presence of epigenetic mechanisms, patients with genetic predispositions have higher probability for suffering from IBD. The most common epigenetic mechanisms in the pathogenesis of IBD are DNA methylation and non-coding RNAs. The epigenetic mechanisms lead to changes in T-cell activity, cytokine production, intestinal epithelial integrity, autophagy activity, and innate immunity response. All of those cause chronic inflammation as the main characteristic of IBD. Genetic aspect can be a promising approach in managing IBD. The field of genetic may be applied in diagnosing, treating, and predicting disease outcomes. However, this topic still needs further investigations.