Institut Pasteur, Unité des Interactions Bactéries-Cellules, Paris, France; Institut National de la Santé et de la Recherche Médicale, U604, Paris, France; Institut National de la Recherche Agronomique, USC2020, Paris, France; Grupo fisiopatología de la Reproducción, Departamento Producción y Sanidad Animal, Salud Pública Veterinaria y Ciencia y Tecnología de los Alimentos, Facultad de Veterinaria, Universidad Cardenal Herrera-CEU, CEU Universities, Valencia, Spain.
Anatomy and Comparative Pathology Department, University of Cordoba, International Excellence Agrifood Campus 'ceiA3,', Córdoba, Spain.
Clin Microbiol Infect. 2019 Feb;25(2):252.e1-252.e4. doi: 10.1016/j.cmi.2018.08.022. Epub 2018 Sep 6.
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.
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.
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).
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.
研究产单核细胞李斯特菌 I 谱系 F2365 菌株表面蛋白内林素 B (InlB) 对毒力的贡献，该菌株于 1985 年在美国加利福尼亚州引发了致命的李斯特菌病暴发。
F2365 菌株显示出一个点突变，阻碍了 InlB 的表达。我们通过在产单核细胞李斯特菌 I 谱系 F2365 的密码子 34 处引入点突变（TAA 至 CAA）来挽救 InlB 的表达。我们使用体外细胞感染系统和小鼠静脉内感染模型研究了它对细菌毒力的重要性。
在 HeLa 和 JEG-3 细胞中，表达 InlB 的 F2365 InlB 菌株的侵袭性分别比 F2365 菌株高约 9 倍和 1.5 倍。在感染后 72 小时感染小鼠的肝脏和脾脏中，F2365 InlB 菌株的细菌计数明显高于 F2365 菌株（约 1 个对数级），组织病理学评估显示 F2365 菌株的坏死灶数量比 F2365 InlB 菌株减少（Mann-Whitney 检验）。
InlB 在 I 谱系李斯特菌感染非妊娠动物的过程中起着关键作用。InlB 中的自发突变可能防止了 1985 年加利福尼亚李斯特菌病暴发时更严重的人类发病率和死亡率。
