ArticleNature communications2026
Engineered bacterial therapy suppresses Enterohemorrhagic Escherichia coli through metabolic competition and virulence silencing.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Review
- Pathogenesis and therapeutic strategies in the interaction between gut microbiota and enterohemorrhagic Escherichia coli infection.FEMS microbiology reviews · 2026Review
- Combating Bacterial Infection with Metabolism-Regulating Nanomaterials.International journal of nanomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.