单核增生李斯特氏菌信息素脂蛋白PplA介导的细菌感染机制

Mechanisms of bacterial infection mediated by the lipoprotein PplA of Listeria monocytogenes

摘要:

目的 利用单核增生李斯特氏菌野生株、脂蛋白基因pplA缺失株和回补株探究PplA在单核增生李斯特氏菌感染功能中的作用。方法 比较野生株、缺失株和回补株在细胞溶血能力、细胞黏附和侵袭能力、胞内增殖能力、胞间迁移能力、小鼠脏器定殖能力、小鼠脏器内细菌毒力因子转录水平和群体感应相关基因转录水平等方面的差异，从而解析PplA在单核增生李斯特氏菌感染宿主中的作用。结果 缺失pplA基因后，单核增生李斯特氏菌的胞内增殖能力和胞间迁移能力无显著差异，但溶血能力、细胞黏附和侵袭能力、小鼠脏器定殖能力均显著降低，且小鼠脏器内细菌毒力因子plcB、hly和prfA的转录水平显著下降。此外，群体感应相关基因agrA、agrB、agrC和luxS的转录水平也发生了显著变化。结论 研究表明单核增生李斯特氏菌脂蛋白PplA参与细菌毒力调控过程，显著影响细菌的致病力。

Abstract:

Objective We employed the wild-type strain of Listeria monocytogenes, the lipoprotein gene pplA- deleted strain, and the complementary strain to investigate the role of PplA in the infection of L. monocytogenes.Methods We compared the hemolytic capacity, cell adhesion and invasion, intracellular proliferation, cell-to-cell migration, mouse organ colonization, transcription levels of virulence factors in mouse organs, and transcription levels of quorum sensing-related genes among wild-type, pplA-deleted, and complementary strains to explore the role of PplA in the infection of L. monocytogenes.Results After the deletion of pplA, L. monocytogenes showed no significant change in intracellular proliferation or cell-to-cell migration. However, its hemolytic capacity, cell adhesion and invasion, mouse organ colonization, and transcription levels of virulence factors such as plcB, hly, and prfA in mouse organs were significantly reduced. Moreover, the transcription levels of quorum sensing-related genes agrA, agrB, agrC, and luxS were altered in the pplA-deleted strain.Conclusion The lipoprotein PplA is involved in the virulence regulation and affects the pathogenicity of L. monocytogenes.