Abstract
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 vivo mouse 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.
Highlights
Autophagy literally means “self-eating.” Autophagy describes a process by which our cells are able to cope with damaged organelles and malformed proteins by directing them to lysosomal degradation
Whether NOD2 mutation was present in the same cells. These findings suggest that the observed impairment in autophagy in the intestine of patients with Crohn’s disease (CD) may occur as a result of a combined defect in NOD2 and ATG16L1
DIRECTIONS In this review, we have discussed in detail, the most important gene pathways that have been shown to be important in mediating autophagy in intestinal homeostasis
Summary
Autophagy literally means “self-eating.” Autophagy describes a process by which our cells are able to cope with damaged organelles and malformed proteins by directing them to lysosomal degradation. Autophagy may be divided into three classes; macroautophagy, macroautophagy, and chaperone-mediated autophagy [1, 2] Of these three classes, macroautophagy, or autophagy, as it will be referred to hereafter, is the most studied and is the form implicated in the regulation of chronic inflammation and is the focus of this review. An additional form of selective autophagy is xenophagy. Xenophagy serves to degrade invasive pathogens in a specialized form of autophagy termed xenophagy [10]. Xenophagy involves the recruitment of the autophagic machinery to degrade invasive viral or bacterial pathogens. The myriad roles of autophagy in regulating homeostasis make it of particular interest in study of the intestinal mucosa, where all the aforementioned stresses are likely to converge
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