Department of Pediatrics, Division of Newborn Medicine, St. Louis Children's Hospital, Washington University School of Medicine, St. Louis, MO, USA.
Department of Pediatrics, Division of Neonatology, Monroe Carell Jr. Children's Hospital at Vanderbilt, Vanderbilt University Medical Center, Nashville, TN, USA.
Semin Fetal Neonatal Med. 2018 Dec;23(6):394-399. doi: 10.1016/j.siny.2018.08.002. Epub 2018 Aug 17.
Necrotizing enterocolitis (NEC) is the most frequent and devastating gastrointestinal disease of premature infants. Although the precise mechanisms are not fully understood, NEC is thought to develop following a combination of prematurity, formula feeding, and adverse microbial colonization. Within the last decade, studies increasingly support an important role of a heightened mucosal immune response initiating a pro-inflammatory signaling cascade, which can lead to the disruption of the intestinal epithelium and translocation of pathogenic species. In this review, we first describe the cellular composition of the intestinal epithelium and its critical role in maintaining epithelial integrity. We then discuss cell signaling during NEC, specifically, toll-like receptors and nucleotide oligomerization domain-like receptors. We further review cytokines and cellular components that characterize the innate and adaptive immune systems and how they interact to support or modulate NEC development.
坏死性小肠结肠炎(NEC)是早产儿最常见和最具破坏性的胃肠道疾病。尽管确切的发病机制尚不完全清楚,但人们认为 NEC 是在早产、配方奶喂养和不良微生物定植的共同作用下发展起来的。在过去的十年中,越来越多的研究支持高度黏膜免疫反应引发促炎信号级联反应的重要作用,这可能导致肠道上皮细胞的破坏和病原物种的易位。在这篇综述中,我们首先描述了肠上皮细胞的细胞组成及其在维持上皮完整性方面的关键作用。然后,我们讨论了 NEC 期间的细胞信号转导,特别是 Toll 样受体和核苷酸寡聚化结构域样受体。我们进一步回顾了表征固有和适应性免疫系统的细胞因子和细胞成分,以及它们如何相互作用以支持或调节 NEC 的发展。