Pathogenesis and therapeutic strategies in the interaction between gut microbiota and enterohemorrhagic Escherichia coli infection.

Enterohemorrhagic Escherichia coli (EHEC) is a major foodborne pathogen that causes hemorrhagic colitis and hemolytic uremic syndrome. Increasing evidence indicates that the gut microbiota plays a central role in modulating EHEC pathogenesis through complex metabolic and signaling networks. Beneficial commensals, including Bifidobacterium, Lactobacillus, and segmented filamentous bacteria, contribute to colonization resistance by competing for nutrients and adhesion sites, producing antimicrobial metabolites, and enhancing epithelial barrier integrity. In contrast, certain species such as Bacteroides thetaiotaomicron and Enterococcus faecalis may promote EHEC virulence by altering intestinal nutrient availability or triggering the expression of virulence genes. Microbiota-derived metabolites, including short-chain fatty acids, succinate, indole, riboflavin, nicotinamide, ethanolamine, and L-malate, act as important regulatory signals that connect microbial metabolism with LEE-mediated virulence pathways. Understanding these host-microbe-pathogen interactions provides a mechanistic basis for developing microbiota-targeted interventions such as probiotics, prebiotics, and fecal microbiota transplantation that enhance colonization resistance and attenuate virulence. Integration of AI-based analytics with multi-omics approaches is expected to facilitate the design of personalized, mechanism-driven therapeutic strategies for the control of EHEC infection.