Toll样受体4介导肠上皮损伤与炎症反应在NEC中作用的研究进展  

Research advances in the mechanism of Toll-like receptor 4 mediated intestinal injury and inflammatory response in necrotizing enterocolitis

作　　者：王佳[1] 蔡成 WANG Jia;CAI Cheng(Department of Neonatology,Shanghai Children’s Hospital,School of Medicine,Shanghai Jiao Tong University,Shanghai 200062,China)

机构地区：[1]上海交通大学医学院附属儿童医院,上海市儿童医院新生儿科,上海200062

出　　处：《细胞与分子免疫学杂志》2025年第1期57-63,共7页Chinese Journal of Cellular and Molecular Immunology

基　　金：2023年“科技兴蒙”上海交通大学行动计划专项项目(2023XYJG0001-01-09);2023年上海市儿童医院院级临床研究培育专项(2023YLY02)。

摘　　要：坏死性小肠结肠炎(NEC)是一种见于早产儿的肠道炎症和坏死性疾病,仍是目前早产儿胃肠道疾病死亡的主要原因,其具体发病机制尚不明确。近年来,大量研究报道Toll样受体4(TLR4)在NEC发病中起到关键作用。早产儿肠上皮细胞大量表达的TLR4与细菌脂多糖(LPS)结合后激活下游信号通路,导致肠上皮完整性破坏和细菌移位,从而引起肠道缺血坏死和炎症反应,并可能迅速进展为严重脓毒血症、多器官功能障碍和死亡。本文就TLR4相关信号通路在NEC患儿肠上皮损伤及炎症反应中的作用机制进行综述,为研究新的NEC治疗作用靶点提供参考。Necrotizing enterocolitis(NEC)is an intestinal inflammatory and necrotic disease seen in premature infants,and remains the leading cause of death resulted from gastrointestinal diseases in premature infants.The specific pathogenesis of NEC is still unclear.In recent years,a lot of studies have reported that Toll-like receptor 4(TLR4)plays a key role in the pathogenesis of NEC.TLR4,which is abundantly expressed in intestinal epithelial cells of premature infants,binds to bacterial lipopolysaccharide(LPS)to activate downstream signaling pathways,leading to disruption of intestinal epithelial integrity and bacterial translocation,resulting in intestinal ischemic necrosis and inflammatory responses,which may rapidly progress to severe sepsis,multiple organ dysfunction,and death.This paper reviews the mechanism of TLR4-related signaling pathways in intestinal epithelial injury and inflammatory responses in newborns with NEC,providing a reference to study new therapeutic targets for NEC.

关 键 词：Toll样受体4(TLR4) 坏死性小肠结肠炎(NEC) 早产儿 肠道屏障 炎症反应 综述 

分 类 号：R392.11[医药卫生—免疫学] R574.5[医药卫生—基础医学] R574.62[文化科学—情报学] G353.11