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新生儿坏死性小肠结肠炎的发病机制。

Pathogenesis of neonatal necrotizing enterocolitis.

作者信息

Lim Joanna C, Golden Jamie M, Ford Henri R

机构信息

Division of Pediatric Surgery, Children's Hospital Los Angeles, 4650 Sunset Blvd., Mailstop #72, Los Angeles, CA, 90027, USA.

出版信息

Pediatr Surg Int. 2015 Jun;31(6):509-18. doi: 10.1007/s00383-015-3697-9. Epub 2015 Apr 9.

Abstract

Although necrotizing enterocolitis (NEC) is the most lethal gastrointestinal disease in the neonatal population, its pathogenesis is poorly understood. Risk factors include prematurity, bacterial colonization, and formula feeding. This review examines how mucosal injury permits opportunistic pathogens to breach the gut barrier and incite an inflammatory response that leads to sustained overproduction of mediators such as nitric oxide and its potent adduct, peroxynitrite. These mediators not only exacerbate the initial mucosal injury, but they also suppress the intestinal repair mechanisms, which further compromises the gut barrier and culminates in bacterial translocation, sepsis, and full-blown NEC.

摘要

尽管坏死性小肠结肠炎(NEC)是新生儿群体中最致命的胃肠道疾病,但其发病机制仍知之甚少。风险因素包括早产、细菌定植和配方奶喂养。本综述探讨了黏膜损伤如何使机会性病原体突破肠道屏障并引发炎症反应,导致一氧化氮及其强效加合物过氧亚硝酸盐等介质持续过量产生。这些介质不仅会加剧最初的黏膜损伤,还会抑制肠道修复机制,进而进一步损害肠道屏障,最终导致细菌移位、败血症和严重的坏死性小肠结肠炎。

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