ArticleNature microbiology2024
Enterococcus faecalis-derived adenine enhances enterohaemorrhagic Escherichia coli Type 3 Secretion System-dependent virulence.
Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Arginine metabolism as a mutualistic strategy in the interaction between Porphyromonas gingivalis and Filifactor alocis.Nature communications · 2026Article
- The McbR transcription factor links the intracellular folate pool to virulence in enterohemorrhagicmBio · 2026Article
- Pathogenesis and therapeutic strategies in the interaction between gut microbiota and enterohemorrhagic Escherichia coli infection.FEMS microbiology reviews · 2026Review
- Ag-CuO Nanozymes Superior to Commercial Silver-Based Dressings: Synergistic Antibacterial Therapy via PTS-Mediated Starvation and Cuproptosis-Like Death.Research (Washington, D.C.) · 2026Article
- Multidrug-ResistantVeterinary sciences · 2025Article
- Enterohemorrhagic E. coli (EHEC) and the microbiome.PLoS pathogens · 2025Article
- Article
- Beyond reductionism: the emerging holistic paradigm in indirect control of pathogen infection.Frontiers in microbiology · 2025Article
- Dual quorum-sensing control of purine biosynthesis drives pathogenic fitness ofbioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Interactions between microbiota and enteric pathogens can promote colonization resistance or enhance pathogenesis. The pathobiont Enterococcus faecalis increases enterohaemorrhagic E. coli (EHEC) virulence by upregulating Type 3 Secretion System (T3SS) expression, effector translocation, and attaching and effacing (AE) lesion formation on enterocytes, but the mechanisms underlying this remain unknown. Using co-infection of organoids, metabolomics, supplementation experiments and bacterial genetics, here we show that co-culture of EHEC with E. faecalis increases the xanthine-hypoxanthine pathway activity and adenine biosynthesis. Adenine or E. faecalis promoted T3SS gene expression, while transcriptomics showed upregulation of adeP expression, which encodes an adenine importer. Mechanistically, adenine relieved High hemolysin activity (Hha)-dependent repression of T3SS gene expression in EHEC and promoted AE lesion formation in an AdeP-dependent manner. Microbiota-derived purines, such as adenine, support multiple beneficial host responses; however, our data show that this metabolite also increases EHEC virulence, highlighting the complexity of pathogen-microbiota-host interactions in the gut.
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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.