Reassessing the role of Internalin B in Listeria monocytogenes virulence using the epidemic strain F2365
Résumé
OBJECTIVES:
We investigated the contribution to virulence of the surface protein Internalin B (InlB) in the L. monocytogenes lineage I strain F2365, which caused in California in 1985 one of the deadliest listeriosis outbreaks.
METHODS:
The F2365 strain displays a point mutation that hampers expression of InlB. We rescued the expression of InlB in the L. monocytogenes lineage I strain F2365 introducing a point mutation in the codon 34 (TAA to CAA) and investigated its importance for bacterial virulence using in vitro cell infection systems and a murine intravenous infection model.
RESULTS:
We show in HeLa and JEG-3 cells that the F2365 InlB+ strain expressing InlB was ≈9-fold and ≈1.5-fold more invasive than F2365, respectively. In livers and spleens of infected mice at 72 h post-infection bacterial counts for F2365 InlB+ were significantly higher compared to the F2365 strain (≈1 log more) and histopathological assessment showed that the F2365 strain displayed a reduced number of necrotic foci compared to the F2365 InlB+ strain (Mann-Whitney test).
CONCLUSIONS:
We describe a critical role for InlB during infection of non-pregnant animals by a L. monocytogenes strain from lineage I. Our study suggests that a spontaneous mutation in InlB could have prevented more severe human morbidity and mortality during the 1985 California listeriosis outbreak.
Domaines
Biologie moléculaire
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