Front. Immunol., 30 September 2013 | doi: 10.3389/fimmu.2013.00301
- 1Mucosal Biology Laboratory, School of Human Life Sciences, University of Tasmania, Launceston, TAS, Australia
- 2Laboratory of Experimental Immunopathology, IRCCS “de Bellis”, Castellana Grotte (BA), Italy
One of the most significant challenges of cell biology is to understand how each type of cell copes with its specific workload without suffering damage. Among the most intriguing questions concerns intestinal epithelial cells in mammals; these cells act as a barrier between the internally protected region and the external environment that is exposed constantly to food and microbes. A major process involved in the processing of microbes is autophagy. In the intestine, through multiple, complex signaling pathways, autophagy including macroautophagy and xenophagy is pivotal in mounting appropriate intestinal immune responses and anti-microbial protection. Dysfunctional autophagy mechanism leads to chronic intestinal inflammation, such as inflammatory bowel disease (IBD). Studies involving a number of in vitro and in vivomouse models in addition to human clinical studies have revealed a detailed role for autophagy in the generation of chronic intestinal inflammation. A number of genome-wide association studies identified roles for numerous autophagy genes in IBD, especially in Crohn’s disease. In this review, we will explore in detail the latest research linking autophagy to intestinal homeostasis and how alterations in autophagy pathways lead to intestinal inflammation.
Keywords: IBD, autophagy, intestinal epithelium, ATG16L1, IRGM
Citation: Randall-Demllo S, Chieppa M and Eri R (2013) Intestinal epithelium and autophagy: partners in gut homeostasis. Front. Immunol. 4:301. doi: 10.3389/fimmu.2013.00301
Received: 08 May 2013; Accepted: 10 September 2013;
Published online: 30 September 2013.
Published online: 30 September 2013.
Edited by:
Yasmin Thanavala, Roswell Park Cancer Institute, USA
Reviewed by:
Wim Van Den Broeck, Ghent University, BelgiumRita Carsetti, Ospedale Pediatrico Bambino Gesù, Italy
Copyright: © 2013 Randall-Demllo, Chieppa and Eri. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Rajaraman Eri, School of Human Life Sciences, University of Tasmania, Locked Bag 1320, Launceston, TAS 7250, Australia e-mail: rderi@utas.edu.au
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