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Background and objectives: Non-typhoidal Salmonella (NTS) are among the most prevalent causes of infectious diarrheal disease in humans and pigs, but also contribute to invasive infections in human infants. Their pathogenicity is conferred by horizontally acquired chromosomal regions, called Salmonella pathogenicity islands (SPIs), encoding sets of effector proteins, which are delivered into the host cell via specific type-three secretion systems. Several in vitro studies identified SPI2 as a requirement for the establishment of a Salmonella containing vacuole (SCV), an intracellular compartment allowing survival and replication inside the host cell.
Materials and methods: We used our newly established mouse model to clarify the role of SPI2 in establishment and progression of systemic NTS infections in the neonate host.
Results: Oral infection with wildtype and SPI2-deficient NTS resulted in similar bacterial loads of the gastrointestinal tract, but re-isolation rates of mutants from systemic organs were significantly decreased. In contrast to the general understanding of SPI2 as prerequisite for SCV formation in vitro, mutants established and maintained SCVs and even grow to high numbers without harming their host cell.
Conclusion: By evaluating 15 isogenic SPI2 effector deficient Salmonella strains, we demonstrate that SifA significantly contributes to the SPI2-dependent phenotype. Its lack seems to prevent transmigration of enterocytes and, finally, systemic spread.