| First Author | Yoon CK | Year | 2026 |
| Journal | Cell Rep | Volume | 45 |
| Issue | 8 | Pages | 117801 |
| PubMed ID | 42606933 | Mgi Jnum | J:391939 |
| Mgi Id | MGI:8402879 | Doi | 10.1016/j.celrep.2026.117801 |
| Citation | Yoon CK, et al. (2026) OmpW-mediated sensing of MUC2 GalNAc contributes to the ileal tropism of Salmonella Typhi. Cell Rep 45(8):117801 |
| abstractText | 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 N-acetylgalactosamine (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 an early step of typhoid pathogenesis and a potential target for prevention. |
