PDF(Pubmed)
Abstract：
Necrotizing enterocolitis (NEC) is one of the most devasting diseases affecting preterm neonates. However, despite a lot of research, NEC\'s pathogenesis remains unclear. It is known that the pathogenesis is a multifactorial process, including (1) a pathological microbiome with abnormal bacterial colonization, (2) an immature immune system, (3) enteral feeding, (3) an impairment of microcirculation, and (4) possibly ischemia-reperfusion damage to the intestine. Overall, the immaturity of the mucosal barrier and the increased expression of Toll-like receptor 4 (TLR4) within the intestinal epithelium result in an intestinal hyperinflammation reaction. Concurrently, a deficiency in counter-regulatory mediators can be seen. The sum of these processes can ultimately result in intestinal necrosis leading to very high mortality rates of the affected neonates. In the last decade no substantial advances in the treatment of NEC have been made. Thus, NEC animal models as well as in vitro models have been employed to better understand NEC\'s pathogenesis on a cellular and molecular level. This review will highlight the different models currently in use to study immunological aspects of NEC.
摘要：
坏死性小肠结肠炎（NEC）是影响早产新生儿的最严重的疾病之一。然而,尽管进行了大量的研究,NEC的发病机制尚不清楚。众所周知，发病机理是一个多因素的过程，包括（1）具有异常细菌定植的病理性微生物组，（2）不成熟的免疫系统，（3）肠内喂养，（3）微循环受损，和(4)可能的肠缺血再灌注损伤。总的来说,粘膜屏障的不成熟和肠上皮内Toll样受体4（TLR4）表达的增加导致肠道炎症过度反应。同时,可以看到反监管调解员的不足。这些过程的总和最终会导致肠坏死，从而导致受影响的新生儿的死亡率很高。在过去十年中，NEC的治疗没有取得实质性进展。因此，已采用NEC动物模型和体外模型来更好地了解NEC在细胞和分子水平上的发病机理。这篇综述将重点介绍目前用于研究NEC免疫学方面的不同模型。
