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

• DOI: 10.1016/j.cmi.2018.08.022
• Publication Date: 2018-09-06T04:24:03Z
• Authors: J.J. Quereda; I.M. Rodríguez-Gómez; J. Meza-Torres; J. Gómez-Laguna; M.A. Nahori; O. Dussurget; L. Carrasco; P. Cossart; J. Pizarro-Cerdá
• Keywords: Strain (injury); Lineage (genetic)

ObjectivesTo investigate the contribution to virulence of surface protein internalin B (InlB) in Listeria monocytogenes lineage I strain F2365, which caused a deadly listeriosis outbreak California 1985.MethodsThe F2365 displays point mutation that hampers expression InlB. We rescued InlB L. by introducing codon 34 (TAA CAA). investigated its importance for bacterial using vitro cell infection systems and murine intravenous model.ResultsIn HeLa JEG-3 cells, InlB+ expressing was ≈9-fold ≈1.5-fold more invasive than respectively. In livers spleens infected mice at 72 hours after infection, counts were significantly higher compared (≈1 log more), histopathologic assessment showed displayed reduced number necrotic foci (Mann-Whitney test).ConclusionsInlB plays critical role during nonpregnant animals from I. A spontaneous could have prevented severe human morbidity mortality 1985 outbreak.