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Cholera

消化

关键词消化 疾病 肠道传染病

词汇介绍

拓展阅读

解析

cholera 英 [ˈkɒlərə] 美 [ˈkɑːlərə]

释义   n. [内科] 霍乱

例句   Cholera as well as viruses like those that cause influenza and AIDS infect these areas. 霍乱就像那些导致流感和艾滋病的病毒一样会感染这些区域。


概述

霍乱(cholera)是由O1和O139群霍乱弧菌(Vibrio cholerae)引起的急性肠道传染病,属三大国际检疫传染病之一,也是我国法定管理的甲类传染病。临床特征为剧烈腹泻、呕吐、大量米泔水样排泄物,水电解质紊乱和周围循环衰竭。 流行病学表现时间分布:霍乱的发病没有明显的季节性变化,但夏秋季发病明显增多。人群分布:霍乱没有明显的年龄、性别、种族的差异。所有人都是本病的易感者。是否会得此病,取决于个人的免疫水平高低和暴露机会的大小。 地理分布:霍乱在地理环境分布上以沿海为主,

A modified cholera toxin B subunit containing an ER retention motif enhances colon epithelial repair via an unfolded protein response复制标题

含有ER保留基序的改良霍乱毒素B亚单位通过未折叠蛋白反应增强结肠上皮修复。

发表时间:2019-09-27

影响因子:5.4

作者: Joshua M. Royal

期刊:The FASEB Journal

Cholera toxin B subunit (CTB) exhibits broad-spectrum biologic activity upon mucosal administration. Here, we found that a recombinant CTB containing an endoplasmic reticulum (ER) retention motif (CTB-KDEL) induces colon epithelial wound healing in colitis via the activation of an unfolded protein response (UPR) in colon epithelial cells. In a Caco2 cell wound healing model, CTB-KDEL, but not CTB or CTB-KDE, facilitated cell migration via interaction with the KDEL receptor, localization in the ER, UPR activation, and subsequent TGF-β signaling. Inhibition of the inositol-requiring enzyme 1/X-box binding protein 1 arm of UPR abolished the cell migration effect of CTB-KDEL, indicating that the pathway is indispensable for the activity. CTB-KDEL's capacity to induce UPR and epithelial restitution or wound healing was corroborated in a dextran sodium sulfate-induced acute colitis mouse model. Furthermore, CTB-KDEL induced a UPR, up-regulated wound healing pathways, and maintained viable crypts in colon explants from patients with inflammatory bowel disease (IBD). In summary, CTB-KDEL exhibits unique wound healing effects in the colon that are mediated by its localization to the ER and subsequent activation of UPR in epithelial cells. The results provide implications for a novel therapeutic approach for mucosal healing, a significant unmet need in IBD treatment.-Royal, J. M., Oh, Y. J., Grey, M. J., Lencer, W. I., Ronquillo, N., Galandiuk, S., Matoba, N. A modified cholera toxin B subunit containing an ER retention motif enhances colon epithelial repair via an unfolded protein response.

译文

霍乱毒素B亚基(CTB)粘膜给药后表现出广谱的生物学活性。在这里,我们发现含有内质网(ER)保留基序(CTB-KDEL)的重组CTB通过激活结肠上皮细胞中未折叠的蛋白应答(UPR)来诱导结肠炎中结肠上皮伤口的愈合。在Caco2细胞伤口愈合模型中,CTB-KDEL而非CTB或CTB-KDE通过与KDEL受体相互作用,ER定位,UPR激活和随后的TGF-β信号传导促进细胞迁移。 UPR的需要肌醇的酶1 / X-box结合蛋白1臂的抑制消除了CTB-KDEL的细胞迁移作用,表明该途径对于该活性是必不可少的。在右旋糖酐硫酸钠诱导的急性结肠炎小鼠模型中,证实了CTB-KDEL诱导UPR和上皮修复或伤口愈合的能力。此外,CTB-KDEL诱导了UPR,上调了伤口的愈合途径,并维持了炎症性肠病(IBD)患者结肠外植体中的隐窝。总之,CTB-KDEL在结肠中表现出独特的伤口愈合效果,这是由其定位于ER以及随后上皮细胞中UPR的激活介导的。该结果为粘膜愈合的新型治疗方法提供了启示,这是IBD治疗中未满足的重要需求。-Royal,JM,Oh,YJ,Grey,MJ,Lencer,WI,Ronquillo,N.,Galandiuk,S.,Matoba, N.含有ER保留基序的修饰的霍乱毒素B亚基通过未折叠的蛋白质应答增强结肠上皮修复。