Inflammatory signaling in necrotizing enterocolitis.
Inflammatory signaling in necrotizing enterocolitis.
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DOI：
10.1016/j.clp.2012.12.008
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发表时间：
2013-03
影响因子：
2.1
通讯作者：
De Plaen IG
中科院分区：
文献类型：
--
作者：
De Plaen IG
坏死性小肠结肠炎（NEC）的发病机制仍然知之甚少。许多因素可能使早产肠易受损伤：1）由于微血管发育不完全或肠血管张力调节不成熟，缺乏足够的底物和O2输送到肠上皮细胞; 2）肠屏障不足; 3）异常细菌定植引发的炎症反应;和4）不成熟的免疫应答，导致对微生物的无效杀死，然后通过上皮移位（图1）。同时，炎症介质的过度产生导致中性粒细胞的募集和随后的组织损伤和坏死。NEC的发病机制复杂，其进展速度相当多变。为了了解这种疾病，研究人员检查了从NEC患者身上切除的组织。然而，由于这些是在疾病的晚期获得的，它们不能提供导致NEC的早期致病事件的线索。因此，动物模型已被使用，并有助于确定NEC中炎症网络的几种介质的作用。在本章中，我们讨论了这些炎症介质的作用的证据，并得出结论，目前统一的假设NEC的发病机制。
The pathogenesis of necrotizing enterocolitis (NEC) remains poorly understood. Many factors potentially predispose the premature intestine to injury: 1) A lack of adequate substrate and O2 delivery to the intestinal epithelial cells, due to an incomplete microvasculature development or to an immature regulation of the intestinal vascular tone; 2) an inadequate intestinal barrier; 3) an inflammatory response triggered by abnormal bacterial colonization; and 4) an immature immune response, leading to inefficient killing of microbes which then translocate through the epithelium (Fig. 1). At the same time, an excessive production of inflammatory mediators leads to the recruitment of neutrophils and subsequent tissue injury and necrosis.The pathogenesis of NEC is complex and its speed of progression is quite variable. In an attempt to gain understanding of the disease, researchers have examined tissues resected from patients with NEC. However, as these are obtained at late stages of the disease, they do not yield clues about the early pathogenic events leading to NEC. Therefore animal models have been used and have helped to identify a role for several mediators of the inflammatory network in NEC. In this chapter, we discuss the evidence for the role of these inflammatory mediators and conclude with a current unifying hypothesis regarding NEC pathogenesis.
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