Journal
CURRENT OPINION IN GASTROENTEROLOGY
Volume 31, Issue 1, Pages 81-88Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MOG.0000000000000144
Keywords
autophagy; Crohn's disease; endoplasmic reticulum stress; inflammatory bowel disease; Paneth cells
Categories
Funding
- NIH [DK044319, DK051362, DK053056, DK088199]
- Harvard Digestive Diseases Center (HDDC) [DK0034854]
- High Point Foundation
- European Research Council (ERC) under the European Community/ERC [260961]
- National Institute for Health Research Cambridge Biomedical Research Centre
- Addenbrooke's Charitable Trust
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK034854, R01DK053056, R01DK051362, R01DK088199, R37DK044319, R01DK044319] Funding Source: NIH RePORTER
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Purpose of review The purpose of this study is to provide an overview of the role of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in inflammatory bowel disease (IBD). Recent findings Human genetic studies have identified several UPR-related genes and autophagy-related genes as IBD risk loci. Impairment of each branch of the UPR causes spontaneous enteritis or creates higher susceptibility for intestinal inflammation in model systems. Deficiency of either UPR or autophagy in small intestinal epithelial cells promotes each other's compensatory engagement, which is especially prominent in Paneth cells such that, in the absence of both, severe spontaneous enteritis emerges. Summary Interactions between the UPR and autophagy exhibit critical synergistic interactions within the intestinal epithelium and especially Paneth cells that are of considerable importance to the maintenance of homeostasis. When dysfunctional in the Paneth cell, spontaneous inflammation can emerge that may extend beyond the epithelium providing direct experimental evidence that subsets of Crohn's disease may emanate from primary Paneth cell disturbances.
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