Narrative review uncovers gut microbiota mechanisms regulating enterohemorrhagic Escherichia coli virulence and colonization, highlighting microbiota-targeted therapeutic interventions.
Key Points
To review the metabolic and signaling interactions between the intestinal microbiota and enterohemorrhagic Escherichia coli (EHEC), and evaluate microbiota-targeted therapeutic strategies.
Synthesized findings on commensal-pathogen nutrient competition, metabolite signaling, and epithelial barrier modulation during EHEC pathogenesis.
Assessed microbiota-modulating interventions including probiotics, prebiotics, fecal microbiota transplantation, and computational multi-omics integration.
Commensals such as Bifidobacterium and Lactobacillus confer colonization resistance by competing for binding sites, producing antimicrobial metabolites, and reinforcing barrier integrity, whereas species like Bacteroides thetaiotaomicron and Enterococcus faecalis enhance pathogen virulence.
Microbiome-derived metabolites, including short-chain fatty acids, succinate, and indole, function as regulatory chemical signals that modulate locus of enterocyte effacement (LEE) virulence gene expression.
Targeted microbiota interventions, such as fecal microbiota transplantation and multi-omics-guided personalized therapies, show potential to attenuate virulence and restore resistance against infection.