Autophagy at the gut interface: Mucosal responses to stress and the consequences for inflammatory bowel diseases

Huett, Alan; Xavier, Ramnik J.

doi:10.1002/ibd.20991

Cited by 23 publications

(20 citation statements)

References 156 publications

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“…Apoptosis and autophagy are two closely connected cellular mechanisms through which aged, superfluous, or damaged cells are eliminated (27). The importance of apoptosis in preservation of intestinal integrity is well established, whereas the role of autophagy is still not fully understood (16).…”

Section: Discussionmentioning

confidence: 99%

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Epidermal growth factor reduces autophagy in intestinal epithelium and in the rat model of necrotizing enterocolitis

Maynard¹,

Dvorak

Khailová³

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Epidermal growth factor (EGF) is one of the most promising candidates in NEC prophylaxis. Autophagy regulates cell homeostasis, but uncontrolled activation of autophagy may lead to cellular injury. The aim was to evaluate the effects of EGF on intestinal autophagy in epithelial cells and in the rat NEC model and measure autophagy in NEC patients. Intestinal epithelial cells (IEC-6) and the rat NEC model were used to study the effect of EGF on intestinal autophagy. Protein levels of Beclin 1 and LC3II were measured in the intestinal epithelium in both in vivo and in vitro models. Ultrastructural changes in intestinal epithelium were studied by electron microscopy. Expression of Beclin 1, LC3II, and p62 protein was evaluated in biopsies from NEC patients. Autophagy was induced in IEC-6 cells and inhibited by adding EGF into the culture. In the rat NEC model, EGF treatment of NEC reduced expression of Beclin 1 and LC3II in ileal epithelium. Morphologically, typical signs of autophagy were observed in the epithelium of the NEC group, but not in the EGF group. A strong signal for Beclin 1 and LC3II was detected in the intestine from patients with NEC. Autophagy is activated in the intestinal epithelium of NEC patients and in the ileum of NEC rats. Supplementation of EGF blocks intestinal autophagy in both in vivo and in vitro conditions. Results from this study indicate that EGF-mediated protection against NEC injury is associated with regulation of intestinal autophagy.

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Section: Discussionmentioning

confidence: 99%

“…Recently, autophagy has been linked to intestinal pathophysiology (16). Results from several studies indicate that the defect of mammalian ATG16L1 and interferon-regulated GTPase (IRGM) genes leads to increased susceptibility for Crohn's disease (29,30).…”

mentioning

confidence: 99%

Epidermal growth factor reduces autophagy in intestinal epithelium and in the rat model of necrotizing enterocolitis

Maynard¹,

Dvorak

Khailová³

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…NS nonsigniWcant; *P < 0.05 the presence of M-cells, which are specialized gateways transporting intact molecules and microorganisms through the epithelium for antigen presentation to the underlying immune cells of the Peyer's patch. This plays a crucial role in the induction of innate immunity through generation of IgA responses (Huett and Xavier 2010). Therefore, we were interested whether CS exposure did induce autophagic changes in M-cells as well.…”

Section: M-cells Are Also Avected By Smoke-induced Autophagymentioning

confidence: 99%

Cigarette smoke and the terminal ileum: increased autophagy in murine follicle-associated epithelium and Peyer’s patches

Verschuere

Allais

Bracke

et al. 2011

Histochem Cell Biol

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Cigarette smoke (CS) exposure is associated with increased autophagy in several cell types, such as bronchial epithelial cells. Smoking is also an environmental risk factor in Crohn's disease, in which impairment of the autophagy-mediated anti-bacterial pathway has been implicated. So far, it is unknown whether CS induces autophagy in the gut. Here, we examined the effect of chronic CS exposure on autophagy in the follicle-associated epithelium (FAE) of murine Peyer's patches. Transmission electron microscopy revealed that the proportion of cell area occupied by autophagic vesicles significantly increased in the FAE after CS exposure. An increased number of autophagic vesicles was observed in the FAE, whereas the vesicle size remained unaltered. Besides enterocytes, also M-cells contain more autophagic vesicles upon CS exposure. In addition, the mRNA level of the autophagy-related protein Atg7 in the underlying Peyer's patches is increased after CS exposure, which indicates that the autophagy-inducing effect of CS is not limited to the FAE. In conclusion, our results demonstrate that CS exposure induces autophagy in murine FAE and in the underlying immune cells of Peyer's patches, suggesting that CS exposure increases the risk for Crohn's disease by causing epithelial oxidative damage, which needs to be repaired by autophagy.

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“…[1][2][3] Autophagy is an evolutionarily conserved process important for recycling organelles and removing unwanted cytoplasmic cargo. 4 Two ubiquitin-like conjugation pathways are required for autophagosome initiation and formation, and autophagy-related gene (Atg)5 is essential in both systems. 4 In brief, following activation by the E1-like enzyme ATG7 and transfer to the E2-like enzyme ATG10, ATG12 becomes conjugated to ATG5.…”

Section: Introductionmentioning

confidence: 99%

“…4 Two ubiquitin-like conjugation pathways are required for autophagosome initiation and formation, and autophagy-related gene (Atg)5 is essential in both systems. 4 In brief, following activation by the E1-like enzyme ATG7 and transfer to the E2-like enzyme ATG10, ATG12 becomes conjugated to ATG5. ATG16L1, which is assembled with the ATG12-ATG5 conjugate, is able to homotetramerize and the ATG12-ATG5-ATG16L1 multimers are recruited to the nascent autophagosomal membrane.…”

Section: Introductionmentioning

confidence: 99%

ATG5 regulates plasma cell differentiation

et al. 2013

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Autophagy at the gut interface: Mucosal responses to stress and the consequences for inflammatory bowel diseases

Cited by 23 publications

References 156 publications

Epidermal growth factor reduces autophagy in intestinal epithelium and in the rat model of necrotizing enterocolitis

Epidermal growth factor reduces autophagy in intestinal epithelium and in the rat model of necrotizing enterocolitis

Cigarette smoke and the terminal ileum: increased autophagy in murine follicle-associated epithelium and Peyer’s patches

ATG5 regulates plasma cell differentiation

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