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调节整合素α5β1介导的黄金葡萄球菌细胞入侵由隔膜细胞骨架
Stevens Robertin1, Dominik Brokatzky1, Damián Lobato-Márquez1
1Department of Infection Biology, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, United Kingdom.
European journal of cell biology
|September 8, 2023
概括
细胞骨架组成部分的septins被招募到金黄色葡萄球菌入侵部位,影响细菌进入宿主细胞. 七面体枯竭会影响整蛋白表达和细菌粘附.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 金黄色葡萄球菌 (Staphylococcus aureus) 是一种重要的细菌病原体,引起各种感染.
- 最初被认为是细胞外的,黄金色杆菌现在被认为是有能力的细胞内病原体.
- 纤维素结合蛋白 (FnBPA/B) 调解金色菌与宿主整合素α5β1的相互作用,促进入侵.
研究的目的:
- 为了调查septins在S. aureus入侵中的作用.
- 确定细菌进入过程中septins如何与宿主细胞机械相互作用.
- 为了阐明整合素α5β1的调节和S. aureus被septins的入侵.
主要方法:
- 使用FnBPA涂层乳珠研究在无细菌系统中的隔膜招募.
- 研究了对S. aureus入侵地点的septin招募.
- 雇佣了SEPT2枯竭,以评估其对S. aureus入侵,整蛋白表达和FAK水平的影响.
主要成果:
- 七蛋白与黄金色细菌入侵部位的活性蛋白相结合,与整蛋白α5β1.1接触.
- 在整合素α5β1激活时,发生了septin招募.
- SEPT2 枯竭减少了细菌入侵,但增加了表面整合蛋白α5表达和黄金色粘性.
结论:
- 七被招募到S. aureus入侵部位,并起到调节细菌进入的作用.
- SEPT2 枯竭会改变整合素α5β1表达和焦粘附激酶 (FAK) 水平,影响细菌的粘附和侵入.
- 这些发现为septins,integrins和S. aureus病原体之间的相互作用提供了新的见解.
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