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OmpW-mediated sensing of MUC2 GalNAc contributes to the ileal tropism of Salmonella Typhi [STm]

ABSTRACT: Salmonella Typhi (STy), the causative agent of typhoid fever, preferentially infects the ileum, but the basis for this preference has remained unknown. We show that STy exploits MUC2-derived monosaccharides, such as GalNAc, to upregulate invasion and target the ileum—opposite to the response of closely related S. Typhimurium (STm), whose invasion is inhibited by MUC2. Three STy-specific extracellular residues of the outer-membrane protein OmpW (K141/T142/Q193) engage GalNAc, and a periplasmic relay through the short FepE_STy, RS12510, and TonB transmits this signal to activate the master invasion regulator HilD. Mice lacking MUC2 or gut microbiota lose STy ileal tropism, which is restored by oral GalNAc-containing monosaccharides. An OmpW triple-mutant STy strain establishes a murine oral STy infection model, identifying STy–MUC2 glycan interactions as one of the earliest steps of typhoid pathogenesis and a potential target for prevention.

ORGANISM(S): Salmonella enterica subsp. enterica serovar Typhimurium

PROVIDER: GSE337685 | GEO | 2026/07/15

REPOSITORIES: GEO

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OmpW-mediated sensing of MUC2 GalNAc contributes to the ileal tropism of Salmonella Typhi [STy]

Project description:Salmonella Typhi (STy), the causative agent of typhoid fever, preferentially infects the ileum, but the basis for this preference has remained unknown. We show that STy exploits MUC2-derived monosaccharides, such as GalNAc, to upregulate invasion and target the ileum—opposite to the response of closely related S. Typhimurium (STm), whose invasion is inhibited by MUC2. Three STy-specific extracellular residues of the outer-membrane protein OmpW (K141/T142/Q193) engage GalNAc, and a periplasmic relay through the short FepE_STy, RS12510, and TonB transmits this signal to activate the master invasion regulator HilD. Mice lacking MUC2 or gut microbiota lose STy ileal tropism, which is restored by oral GalNAc-containing monosaccharides. An OmpW triple-mutant STy strain establishes a murine oral STy infection model, identifying STy–MUC2 glycan interactions as one of the earliest steps of typhoid pathogenesis and a potential target for prevention.

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