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Updated: Jan 18, 2026

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Enterococcus faecalis的氧化还原代谢激活了未折叠的蛋白质反应,以损害伤口愈合
Aaron Ming Zhi Tan1,2, Cenk Celik1, Stella Yue Ting Lee1
1School of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
Science advances
|January 16, 2026
概括
肠球菌使用细胞外电子运输 (EET) 来产生活性氧物种 (ROS),触发未折叠蛋白质反应 (UPR) 并延迟伤口愈合. 这一发现为慢性感染提供了新的治疗点.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 菌 (Enterococcus faecalis) 是一种机会性病原体,经常在与生物膜相关的感染中发现.
- 通过E. faecalis损害宿主组织反应,特别是伤口愈合的机制仍然不太清楚.
研究的目的:
- 研究细胞外电子传输 (EET) 在E. faecalis病毒性中所起的作用.
- 阐明E. faecalis如何影响宿主上皮细胞反应和伤口修复.
主要方法:
- 研究了细胞外电子传输 (EET) 作为E. faecalis.中反应性氧物种 (ROS) 的来源.
- 评估了E. faecalis衍生的ROS对上皮细胞未折叠蛋白反应 (UPR) 和迁移的影响.
- 用于ROS排毒的催化酶和外源氧化物调节ET缺乏菌株的UPR.
- 研究了药理性UPR抑制对上皮细胞迁移的影响.
主要成果:
- 确定了EET作为E. faecalis.中的ROS的新来源.
- 证明E. faecalis诱导的ROS直接触发上皮细胞中的UPR,导致细胞迁移延迟.
- 通过催化剂的ROS解毒挽救了上皮细胞的迁移,并抑制了UPR.
- 外源性过氧化在ET缺乏菌株中恢复了UPR,证实了ROS-UPR的联系.
- UPR中断损害了上皮细胞迁移,强调了它在伤口修复中的重要性.
结论:
- 在E. faecalis中,细胞外电子传输 (EET) 是一种与宿主细胞通过ROS产生压力相关的毒性机制.
- 细菌ROS诱导的UPR严重损害了上皮细胞的迁移,并延迟了伤口愈合.
- 准细菌ET或UPR通路为慢性E. faecalis感染提供了新的治疗策略.
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