Endoplasmic reticulum stress and intestinal inflammation.
Endoplasmic reticulum stress and intestinal inflammation.
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内质网应激与肠道炎症
DOI：
10.1038/mi.2009.122
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发表时间：
2010-01
影响因子：
8
通讯作者：
Blumberg RS
中科院分区：
文献类型：
--
作者：
Kaser A;Blumberg RS
肠上皮细胞（IEC）作为肠道微生物群和肠道免疫系统之间的重要中介，越来越被认为发挥着重要作用。此外，现在认识到，炎症性肠病（IBD）中的肠道炎症可能主要由IEC功能障碍引起，IEC功能障碍是由于X盒结合蛋白-1功能的遗传破坏导致的未解决的内质网（ER）应激所致。除了未折叠蛋白反应的主要（遗传）异常外，各种次要（炎症和环境）因素也可能是ER应激的重要调节因子。众所周知，ER应激途径也可以调节自噬途径（并被自噬途径调节）。因此，宿主处理内质网应激的能力可能是主要由IEC引起的肠道炎症发病机制的主要途径。在此，我们讨论了在IEC的ER应激作为一个发起人和肠炎症在IBD的延续。
The intestinal epithelial cell (IEC) is increasingly recognized to play a prominent role as an important intermediary between the commensal microbiota and the intestinal immune system. Moreover, it is now recognized that intestinal inflammation in inflammatory bowel disease (IBD) may arise primarily from IEC dysfunction due to unresolved endoplasmic reticulum (ER) stress as a consequence of genetic disruption of X box binding protein-1 function. In addition to primary (genetic) abnormalities of the unfolded protein response, a variety of secondary (inflammation and environmental) factors are also likely to be important regulators of ER stress. ER stress pathways are also well known to regulate (and be regulated by) autophagy pathways. Therefore, the host’s ability to manage ER stress is likely to be a major pathway in the pathogenesis of intestinal inflammation that arises primarily from the IEC. Herein we discuss ER stress in the IEC as both an originator and perpetuator of intestinal inflammation in IBD.