Link to Pubmed [PMID] – 30195066
Clin. Microbiol. Infect.
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.https://www.ncbi.nlm.nih.gov/pubmed/30195066