Reassessing the role of internalin B in Listeria monocytogenes virulence using the epidemic strain F2365.

ABSTRACT:

Objectives

To investigate the contribution to virulence of the surface protein internalin B (InlB) in the Listeria monocytogenes lineage I strain F2365, which caused a deadly listeriosis outbreak in California in 1985.

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 by introducing a point mutation in the codon 34 (TAA to CAA). We investigated its importance for bacterial virulence using in vitro cell infection systems and a murine intravenous infection model.

Results

In HeLa and JEG-3 cells, 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 hours after infection, bacterial counts for F2365 InlB⁺ were significantly higher compared to the F2365 strain (?1 log more), and histopathologic assessment showed that the F2365 strain displayed a reduced number of necrotic foci compared to the F2365 InlB⁺ strain (Mann-Whitney test).

Conclusions

InlB plays a critical role during infection of nonpregnant animals by a L. monocytogenes strain from lineage I. A spontaneous mutation in InlB could have prevented more severe human morbidity and mortality during the 1985 California listeriosis outbreak.

SUBMITTER: Quereda JJ 

PROVIDER: S-EPMC6365677 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature