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Article Dans Une Revue Clinical Microbiology and Infection Année : 2019

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

Résumé

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.

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Bactériologie
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Dates et versions

pasteur-01890600 , version 1 (08-10-2018)
pasteur-01890600 , version 2 (14-05-2020)

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J J Quereda, I M Rodríguez-G Omez, J Meza-Torres, Jaime Gomez-Laguna, Marie-Anne Nahori, et al.. Reassessing the role of internalin B in Listeria monocytogenes virulence using the epidemic strain F2365. Clinical Microbiology and Infection, 2019, 25 (2), pp.252.E1-252.E4. ⟨10.1016/j.cmi.2018.08.022⟩. ⟨pasteur-01890600v2⟩
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