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<p>Enterohemorrhagic <i>Escherichia coli</i> (EHEC) is a severe foodborne pathogen that can lead to hemolytic uremic syndrome. However, antibiotics are contraindicated for EHEC treatment due to toxin release and gut microbiota disruption. Here we report a dual‑mechanism therapeutic strategy combining an engineered <i>Escherichia coli</i> Nissle 1917 strain (EcN3) with 2′‑fucosyllactose (2‑FL) delivered via multicompartment microspheres (MCMs). EcN3 expresses α‑L‑fucosidase to hydrolyze 2‑FL into lactose and fucose. Lactose enhances glucuronic acid utilization, limiting a preferred nutrient of EHEC, whereas fucose activates FusKR signaling to suppress virulence gene expression. MCMs confer gastric protection and enable targeted colonic release, ensuring coordinated activity. In female mouse models and infant rabbit models of <i>Citrobacter rodentium</i> and EHEC infection, this system reduces intestinal colonization, virulence gene expression and epithelial damage without inducing Shiga toxin production. Moreover, MCMs-based strategy preserves the relative abundance of <i>Lactobacillus</i>, and promotes intestinal integrity. This targeted strategy presents a viable alternative to antibiotics, addressing EHEC pathogenesis and antibiotic resistance.</p>

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Engineered bacterial therapy suppresses Enterohemorrhagic Escherichia coli through metabolic competition and virulence silencing

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月3日

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  • Guozhen Ma,
  • Ruiying Liu,
  • Xueping Li,
  • Jialin Wu,
  • Yuanyuan Niu,
  • Sheng Wang,
  • Ziwei Chen,
  • Xudong Qin,
  • Qian Wang,
  • Junyue Wang,
  • Jiamin Qian,
  • Mingqing Zhang,
  • Yu Pang,
  • Yamin Sun,
  • Guosheng Tang,
  • Tao Wang,
  • Yutao Liu

摘要

Enterohemorrhagic Escherichia coli (EHEC) is a severe foodborne pathogen that can lead to hemolytic uremic syndrome. However, antibiotics are contraindicated for EHEC treatment due to toxin release and gut microbiota disruption. Here we report a dual‑mechanism therapeutic strategy combining an engineered Escherichia coli Nissle 1917 strain (EcN3) with 2′‑fucosyllactose (2‑FL) delivered via multicompartment microspheres (MCMs). EcN3 expresses α‑L‑fucosidase to hydrolyze 2‑FL into lactose and fucose. Lactose enhances glucuronic acid utilization, limiting a preferred nutrient of EHEC, whereas fucose activates FusKR signaling to suppress virulence gene expression. MCMs confer gastric protection and enable targeted colonic release, ensuring coordinated activity. In female mouse models and infant rabbit models of Citrobacter rodentium and EHEC infection, this system reduces intestinal colonization, virulence gene expression and epithelial damage without inducing Shiga toxin production. Moreover, MCMs-based strategy preserves the relative abundance of Lactobacillus, and promotes intestinal integrity. This targeted strategy presents a viable alternative to antibiotics, addressing EHEC pathogenesis and antibiotic resistance.