Abstract
Technological and conceptual advances in inflammatory bowel disease research have uncovered new mechanisms that contribute to the pathogenesis of these disorders. It is becoming increasingly clear that the microbiota of the gut and the response of intestinal cells to that microbiota can initiate or contribute to intestinal inflammation. Evidence from genetic studies have identified IBDassociated genes implicated in autophagy and innate sensing of microbes. These genes also play key roles in the homeostasis of a cell type that stands at the interface of host-microbial interaction - the Paneth cell. Here we discuss recent findings that underscore the importance of the microbiome, Paneth cells and autophagy in inflammatory bowel disease.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 146-152 |
| Number of pages | 7 |
| Journal | Current gastroenterology reports |
| Volume | 14 |
| Issue number | 2 |
| DOIs | |
| State | Published - Apr 2012 |
Funding
Disclosure Dr. D. Boone has received grant support from the Crohn’s and Colitis Foundation of America and the National Institutes of Health; Drs. J. Kwon and S. Murphy reported no potential conflicts of interest relevant to this article.
Keywords
- ATG16L1
- Autophagy
- Crohn's disease
- ER Stress
- IRGM
- Microbiome
- NOD2
- Novel regulator pathways
- Paneth cell
- Ulcerative colitis
- Unfolded protein response
ASJC Scopus subject areas
- Gastroenterology