Iron and intestinal immunity.
Iron and intestinal immunity.
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DOI：
10.1097/mog.0b013e32834a4cd1
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发表时间：
2011-10
影响因子：
2.5
通讯作者：
Shanmugam NN
中科院分区：
文献类型：
--
作者：
Cherayil BJ;Ellenbogen S;Shanmugam NN
铁代谢研究的最新进展使人们对铁与炎症反应相互作用的分子基础有了更好的了解。我们将在胃肠道的背景下回顾这一新信息。铁对肠道微生物病原体的作用是众所周知的。最近的研究表明，铁对肠道微生物群也有潜在的重要影响。在宿主方面，hepcidin是哺乳动物铁代谢的关键调节因子，已成为铁稳态和炎症之间交叉对话的重要中介。hepcidin依赖性铁通量的改变可以影响炎症因子的表达，反过来，炎症因子可以诱导hepcidin表达并改变铁稳态。在炎症性肠病的一些研究中发现Hepcidin水平升高，而在这种疾病的动物模型中操纵Hepcidin表达对炎症和铁代谢失调都有有益的影响。近年来获得的铁代谢信息为胃肠道炎症性疾病的发病机制提供了新的线索，也开始提出治疗此类疾病的新方法。
Recent advances in the study of iron metabolism have led to a better understanding of the molecular basis for the interactions between iron and the inflammatory response. We will review this new information in the context of the gastrointestinal tract. The effects of iron on microbial enteropathogens are well known. Recent work has demonstrated that iron also has potentially important effects on the intestinal microbiota. On the host side, hepcidin, a key regulator of mammalian iron metabolism, has emerged as an important mediator of the cross-talk between iron homeostasis and inflammation. Hepcidin-dependent changes in iron flux can influence the expression of inflammatory cytokines, and conversely, inflammatory cytokines can induce hepcidin expression and alter iron homeostasis. Hepcidin levels have been found to be elevated in some studies of inflammatory bowel disease, while manipulating hepcidin expression in animal models of this condition has beneficial effects on both inflammation and dysregulated iron metabolism. The information on iron metabolism that has become available in recent years has shed new light on the pathogenesis of inflammatory diseases of the gastrointestinal tract, and is also starting to suggest new approaches to treating such diseases.