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基因工程表达IL-34的细菌通过促进肠粘膜上皮细胞中紧密结 protein的表达来缓解DSS诱导的实验性结肠炎

Weijie Chen¹, Tongtong Zhou¹, Yicun Liu²

¹Medical School, Nantong University, Nantong, Jiangsu Province 226001, China.

Molecular immunology

|January 26, 2025

概括

通过增强肠道屏障功能,提供介素-34 (IL-34) 的工程细菌提供了对实验性结肠炎的保护. 这表明IL-34是性结肠炎 (UC) 的有前途的治疗标.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
微生物学微生物学

背景情况:

在性结肠炎 (UC) 患者的肠道粘膜中增加了互白素-34 (IL-34).
缺少IL-34会加剧小鼠实验性结肠炎的情况.
缺乏关于直接上调IL-34用于结肠炎治疗的研究.

研究的目的:

在实验性结肠炎中研究直接上调肠道IL-34的治疗潜力.
在大肠炎的小鼠模型中评估表达IL-34的基因工程细菌的疗效.

主要方法:

经过基因工程改造的Escherichia coli Nissle 1917 (EcN) 用于表达CSF-1 (EcN/CSF-1) 或IL-34 (EcN/IL-34).
每天向DSS诱导的大肠炎小鼠注射PBS,EcN/WT,EcN/CSF-1或EcN/IL-34.
评估了临床症状,体重,DAI,肠道透性和组织学/免疫组织学变化;在体外和UC患者样本中评估了紧结蛋白.

主要成果:

埃克N/IL-34测量显著保护小鼠免受DSS诱导的大肠炎.
在 EcN/IL-34 组中改善了结肠组织学损伤和增加了紧结蛋白 (ZO-1,Occludin).
在NCM460细胞中,IL-34上调了紧结蛋白,并与UC上皮细胞中紧结蛋白表达呈正相关性.

结论:

EcN/IL-34 直接作用于受损的肠粘膜,对IL-34 和紧结蛋白进行上调,缓解实验性结肠炎.
IL-34显示出作为性结肠炎的治疗标的潜力.
基因工程表达细胞因子的细菌为UC提供了新的治疗策略.

关键词:

埃舍里奇亚大肠杆菌尼斯尔191717年基因工程细菌是一种基因工程细菌.炎症性肠病是一种炎症性肠病.互乐金-34的使用方法肠道粘膜屏障肠道粘膜屏障紧连接蛋白质的紧连接蛋白质.

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