{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337685/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Salmonella enterica subsp. enterica serovar Typhimurium"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE337685"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"OmpW-mediated sensing of MUC2 GalNAc contributes to the ileal tropism of Salmonella Typhi [STm]","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.","dates":{"publication":"2026/07/15"},"accession":"GSE337685","cross_references":{"GSM":["GSM9859489","GSM9859488","GSM9859485","GSM9859484","GSM9859487","GSM9859486"],"GPL":["37034"],"GSE":["337685"],"taxon":["Salmonella enterica subsp. enterica serovar Typhimurium"]}}