201. Reassessing the role of internalin B in Listeria monocytogenes virulence using the epidemic strain F2365.
- Author
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Quereda JJ, Rodríguez-Gómez IM, Meza-Torres J, Gómez-Laguna J, Nahori MA, Dussurget O, Carrasco L, Cossart P, and Pizarro-Cerdá J
- Subjects
- Animals, Bacterial Proteins genetics, Cell Line, Epidemics, Gene Expression Regulation, Bacterial, Humans, Listeria monocytogenes genetics, Listeria monocytogenes metabolism, Listeriosis epidemiology, Liver microbiology, Membrane Proteins genetics, Mice, Point Mutation, Spleen microbiology, Virulence, Bacterial Proteins metabolism, Listeria monocytogenes pathogenicity, Listeriosis microbiology, Membrane Proteins metabolism
- 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., (Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.)- Published
- 2019
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