Modulatory mechanisms of enterocyte apoptosis by viral, bacterial and parasitic pathogens

被引:16
作者
Buret, Andre G. [1 ]
Bhargava, Amol [1 ]
机构
[1] Univ Calgary, Dept Biol Sci, Calgary, AB T2N 1N4, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Epithelial cell death; Escherichia coli; Giardia; rotavirus; Shigella; ENTEROPATHOGENIC ESCHERICHIA-COLI; CLOSTRIDIUM-DIFFICILE TOXIN; INTESTINAL EPITHELIAL-CELLS; SGLT-1-MEDIATED GLUCOSE-UPTAKE; HELICOBACTER-PYLORI INFECTION; PROTEINASE-ACTIVATED RECEPTOR-2; CASPASE-DEPENDENT APOPTOSIS; IRRITABLE-BOWEL-SYNDROME; LIVER-ABSCESS FORMATION; TIGHT JUNCTIONAL ZO-1;
D O I
10.3109/1040841X.2012.746952
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Enterocyte turnover along with proper epithelial barrier function are crucial aspects of mucosal defense. Apoptosis is a highly regulated type of programmed cell death that allows for the homeostatic turnover of the epithelial layer. Recent studies have suggested that microbial modulation of enterocyte apoptosis can result in increased epithelial permeability, leading to gastrointestinal pathophysiology. In this review, we highlight key mechanisms and pathways via which various viral, bacterial and parasitic pathogens are able to modulate enterocyte apoptosis. We also discuss how these alterations to enterocyte apoptosis can result in the activation of chronic gastrointestinal disorders, such as allergies, irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). The role of proteinase-activated receptors in the pathogenesis of modulated apoptosis-induced pathogenesis is also discussed. Newly discovered processes, through which host epithelial cells may have evolved, rescue mechanisms from microbe-induced apoptosis are discussed. Together, these mechanisms are key to our ever-increasing understanding of host-microbe interactions in the gut.
引用
收藏
页码:1 / 17
页数:17
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