Mihi Belgacem, Good Misty
Division of Newborn Medicine, Department of Pediatrics, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8208, St Louis, MO 63110, USA.
Division of Newborn Medicine, Department of Pediatrics, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8208, St Louis, MO 63110, USA; Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8208, St Louis, MO 63110, USA.
Clin Perinatol. 2019 Mar;46(1):145-157. doi: 10.1016/j.clp.2018.09.007. Epub 2018 Dec 20.
Necrotizing enterocolitis (NEC) remains a leading cause of preterm infant mortality. NEC is multifactorial and believed a consequence of intestinal immaturity, microbial dysbiosis, and an exuberant inflammatory response. Over the past decade, exaggerated Toll-like receptor 4 (TLR4) activity in the immature intestine of preterm neonates emerged as an inciting event preceding NEC. Increased TLR4 signaling in epithelial cells results in the initiation of an uncontrolled immune response and destruction of the mucosal barrier. This article discusses the state of the science of the molecular mechanisms involved in TLR4-mediated inflammation during NEC and the development of new therapeutic strategies to prevent NEC.
坏死性小肠结肠炎(NEC)仍然是早产婴儿死亡的主要原因。NEC是多因素的,被认为是肠道不成熟、微生物生态失调和过度炎症反应的结果。在过去十年中,早产新生儿未成熟肠道中Toll样受体4(TLR4)活性的过度增强成为NEC之前的一个激发事件。上皮细胞中TLR4信号的增加导致不受控制的免疫反应的启动和黏膜屏障的破坏。本文讨论了NEC期间TLR4介导的炎症所涉及的分子机制的科学现状以及预防NEC的新治疗策略的发展。