ArticleNature communications2023
Enterohaemorrhagic E. coli utilizes host- and microbiota-derived L-malate as a signaling molecule for intestinal colonization.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 20 citations in OpenAlex.
- Catabolism of serine enantiomers represses enterohemorrhagicProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Controlled release of coated antioxidants inhibits Citrobacter rodentium colonization in the colon of rats by reducing gut redox potential.Redox biology · 2026Article
- Succinate-driven virulence enhancement in hypervirulentMicrobiology spectrum · 2026Article
- Pathogenesis and therapeutic strategies in the interaction between gut microbiota and enterohemorrhagic Escherichia coli infection.FEMS microbiology reviews · 2026Review
- Inhibition ofMicroorganisms · 2025Article
- Available phosphorus and opportunistic pathogens drive geographic variation in Escherichia coli O157:H7 survival in soils across eastern China.Nature food · 2025Article
- Convergent evolution of distinct D-ribulose utilisation pathways in attaching and effacing pathogens.Nature communications · 2025Article
- Key roles of two-component systems in intestinal signal sensing and virulence regulation in enterohemorrhagic Escherichia coli.FEMS microbiology reviews · 2024Review
- A master regulator of central carbon metabolism directly activates virulence gene expression in attaching and effacing pathogens.PLoS pathogens · 2024Article
- Metabolism of L-arabinose converges with virulence regulation to promote enteric pathogen fitness.Nature communications · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mammalian gastrointestinal tract is a complex environment that hosts a diverse microbial community. To establish infection, bacterial pathogens must be able to compete with the indigenous microbiota for nutrients, as well as sense the host environment and modulate the expression of genes essential for colonization and virulence. Here, we found that enterohemorrhagic Escherichia coli (EHEC) O157:H7 imports host- and microbiota-derived L-malate using the DcuABC transporters and converts these substrates into fumarate to fuel anaerobic fumarate respiration during infection, thereby promoting its colonization of the host intestine. Moreover, L-malate is important not only for nutrient metabolism but also as a signaling molecule that activates virulence gene expression in EHEC O157:H7. The complete virulence-regulating pathway was elucidated; the DcuS/DcuR two-component system senses high L-malate levels and transduces the signal to the master virulence regulator Ler, which in turn activates locus of enterocyte effacement (LEE) genes to promote EHEC O157:H7 adherence to epithelial cells of the large intestine. Disruption of this virulence-regulating pathway by deleting either dcuS or dcuR significantly reduced colonization by EHEC O157:H7 in the infant rabbit intestinal tract; therefore, targeting these genes and altering physiological aspects of the intestinal environment may offer alternatives for EHEC infection treatment.
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