细菌聚合促进了Listeria monocytogenes的内部介导入侵
Liam Feltham1, Josephine Moran1, Marie Goldrick1
1School of Biology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, United Kingdom.
Frontiers in cellular and infection microbiology
|July 24, 2024
概括
李斯特菌使用细菌聚合来入侵宿主细胞,通过ActA和内部蛋白B (InlB) 增强粘附和入侵. 这一策略涉及代谢适应和病毒性基因上调.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 传染性疾病 传染性疾病
背景情况:
- 通过食物传播的病原体Listeria monocytogenes的入侵依赖于内部蛋白质.
- 内部B (InlB) 介导入侵的机制尚不清楚.
研究的目的:
- 阐明Listeria monocytogenes通过InlB介导的入侵机制.
- 研究细菌聚合在宿主细胞入侵中的作用.
主要方法:
- 活细胞显微镜观察宿主-病原体相互作用.
- 使用actA-ΔC突变体研究聚合缺陷细菌.
- RNA测序 (RNA-seq) 用于分析细菌的适应性反应.
主要成果:
- L. monocytogenes 在细胞外环境中形成聚合物,使宿主细胞的粘附率增加了5倍.
- 与非聚合突变物相比,细菌聚合物促进了细胞内入侵的数量增加了3倍.
- 聚合与MET氨酸激酶受体聚类相关,这是InlB介导入侵的标志物.
- RNA-seq揭示了适应性反应,包括铁耗尽,代谢变化和PrfA regulon上调.
结论:
- 细菌聚合是L. monocytogenes入侵的一个关键策略,由PrfA和ActA调解.
- 聚合通过促进宿主细胞粘附和受体聚类来增强InlB介导的入侵.
- L. monocytogenes对宿主环境表现出全局适应性反应,优化了入侵.
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