Review
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 21, 2017; 23(11): 1944-1953
Published online Mar 21, 2017. doi: 10.3748/wjg.v23.i11.1944
Role of autophagy in the pathogenesis of inflammatory bowel disease
Tomoya Iida, Kei Onodera, Hiroshi Nakase
Tomoya Iida, Kei Onodera, Hiroshi Nakase, Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Hokkaido 060-8556, Japan
Author contributions: All authors helped to perform the research; Iida T wrote the paper; all authors have approved the final draft of the manuscript.
Conflict-of-interest statement: No potential conflicts of interest. No financial support.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Hiroshi Nakase, Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Minami 1-jo Nishi 16-chome, Chuo-ku, Sapporo, Hokkaido 060-8556, Japan. hiropynakase@gmail.com
Telephone: +81-11-6112111 Fax: +81-11-6112282
Received: December 28, 2016
Peer-review started: December 29, 2016
First decision: January 19, 2017
Revised: February 7, 2017
Accepted: March 2, 2017
Article in press: March 2, 2017
Published online: March 21, 2017
Abstract

Inflammatory bowel disease (IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system. Recently, some studies provided strong evidence that the process of autophagy affects several aspects of mucosal immune responses. Autophagy is a cellular stress response that plays key roles in physiological processes, such as innate and adaptive immunity, adaptation to starvation, degradation of aberrant proteins or organelles, antimicrobial defense, and protein secretion. Dysfunctional autophagy is recognized as a contributing factor in many chronic inflammatory diseases, including IBD. Autophagy plays multiple roles in IBD pathogenesis by altering processes that include intracellular bacterial killing, antimicrobial peptide secretion by Paneth cells, goblet cell function, proinflammatory cytokine production by macrophages, antigen presentation by dendritic cells, and the endoplasmic reticulum stress response in enterocytes. Recent studies have identified susceptibility genes involved in autophagy, such as NOD2, ATG16L1, and IRGM, and active research is ongoing all over the world. The aim of this review is a systematic appraisal of the current literature to provide a better understanding of the role of autophagy in the pathogenesis of IBD. Understanding these mechanisms will bring about new strategies for the treatment and prevention of IBD.

Keywords: Autophagy, Inflammatory bowel disease, Genome-wide association study, Ulcerative colitis, Crohn’s disease

Core tip: Recent studies provide strong evidence that the process of autophagy affects several aspects of mucosal immune responses. Autophagy is a cellular stress response that plays key roles in physiological processes. Dysfunctional autophagy is recognized as a contributing factor in many chronic inflammatory diseases, including inflammatory bowel disease (IBD). Autophagy plays multiple roles in IBD pathogenesis. Recent studies have identified susceptibility genes involved in autophagy, such as NOD2, ATG16L1, and IRGM, and active research is ongoing around the world. The aim of this review is a systematic appraisal of current literature to provide a better understanding of the role of autophagy in IBD pathogenesis.