Systemic exposure to typhoid toxin primes the murine vascular endothelium for intestinal perforation during Salmonella Typhi infection.

Systemic PltC typhoid toxin exposure primes murine vascular endothelium, making otherwise resistant mice susceptible to oral Salmonella Typhi and causing lethal Peyer’s patch intestinal perforation.

• Why it matters: Intestinal perforation is a late, fatal complication in typhoid fever, yet the mechanism linking toxin exposure to intestinal barrier failure has been unclear.
• What they did: Mice received sequential PltC toxin exposure followed by oral Salmonella Typhi infection to model late-stage human typhoid; endothelial priming was tested with endothelial-specific CMAH expression and by requiring SPI-1 versus SPI-2 T3SS.
• The result: Primed mice developed vascular injury, haemorrhage, and lethal perforation localized to Peyer’s patches, with blood showing microbiota-derived taxa consistent with translocation; lethality depended on SPI-1 T3SS, not SPI-2, and was blocked by CMAH masking Neu5Ac receptors.

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