Sha Sumei, Gao Huijun, Zeng Hong, Chen Fenrong, Kang Junxiu, Jing Yan, Liu Xin, Xu Bin
Department of Gastroenterology, the Second Affiliated Hospital of Xi'an Jiaotong University, Key Laboratory of Gastrointestinal Motility Disorders, Clinical Research Center of Gastrointestinal Diseases, Xi'an, Shaanxi Province 710004, PR China.
Department of Gastroenterology, No. 988 Hospital of Joint Logistic Support Force, Jiaozuo, Henan Province 454000, PR China.
Arab J Gastroenterol. 2024 Nov;25(4):383-389. doi: 10.1016/j.ajg.2024.07.011. Epub 2024 Jul 27.
Adherent invasive Escherichia coli (AIEC) are enriched in IBD (inflammatory bowel disease) patients, but the role and mechanism of AIEC in the intestinal epithelial barrier is poorly defined. We evaluated the role of the AIEC strain E. coli LF82 in vitro and investigated the role of Th17 in this process.
After coincubation with AIEC, the epithelial barrier integrity was monitored by epithelial resistance measurements. The permeability of the barrier was evaluated by TEER (trans-epithelial electrical resistance) and mucosal-to-serosal flux rate. The presence of interepithelial tight junction proteins ZO-1 and Claudin-1 were determined by immunofluorescence and western blot analysis. Cytokines in the cell culture supernatant were assayed by enzyme-linked immunosorbent assay (ELISA).
AIEC infection decreased TEER and increased the mucosal-to-serosal flux rate of Lucifer yellow in the intestinal barrier model in a time- and dose-dependent manner. AIEC infection decreased the expression and changed the distribution of ZO-1 and claudin-1. It also induced the secretion of cytokines such as TNF-α and IL-17.
AIEC strain E. coli LF82 increased the permeability and disrupted the tight junctions of the intestinal epithelial barrier, revealing that AIEC plays an aggravative role in the inflammatory response.
黏附侵袭性大肠杆菌（AIEC）在炎症性肠病（IBD）患者中富集，但AIEC在肠道上皮屏障中的作用及机制尚不清楚。我们在体外评估了AIEC菌株大肠杆菌LF82的作用，并研究了Th17在此过程中的作用。
与AIEC共孵育后，通过测量上皮电阻监测上皮屏障完整性。通过跨上皮电阻（TEER）和黏膜到浆膜通量率评估屏障的通透性。通过免疫荧光和蛋白质印迹分析确定上皮细胞紧密连接蛋白ZO-1和Claudin-1的存在。通过酶联免疫吸附测定（ELISA）检测细胞培养上清液中的细胞因子。
在肠道屏障模型中，AIEC感染以时间和剂量依赖性方式降低TEER并增加荧光素黄的黏膜到浆膜通量率。AIEC感染降低了ZO-1和Claudin-1的表达并改变了其分布。它还诱导了TNF-α和IL-17等细胞因子的分泌。
AIEC菌株大肠杆菌LF82增加了肠道上皮屏障的通透性并破坏了紧密连接，表明AIEC在炎症反应中起加重作用。
