主体PIK3C3促进Shigella flexneri通过真空球形成从细胞传播到细胞
Steven J Rolland1, Zachary J Lifschin1, Erin A Weddle1
1Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia, United States of America.
PLoS pathogens
|May 16, 2025
概括
PIK3C3对于Shigella flexneri的细胞间传播至关重要,使空洞状突起能够成熟成为双膜空洞. 抑制PIK3C3可以减少感染在细胞和幼的传播.
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:
- 石格拉柔性菌通过入侵结肠上皮细胞并在它们之间传播,导致细菌性痢疾.
- 这种细胞对细胞的传播涉及基于actin的运动性,形成膜突起,这些突起分解为真空状突起 (VLPs) 和最终的双膜真空 (DMVs).
研究的目的:
- 为了确定Shigella flexneri细胞间传播至关重要的宿主因素.
- 阐明PIK3C3在真空状突起到双膜真空过渡中的作用.
主要方法:
- 使用HT-29细胞和一个婴儿子模型的石病.
- 采用活光共聚焦显微镜来追踪细菌传播和真空球动态.
- 研究了PIK3C3抑制对感染焦点大小和细菌传播的作用.
主要成果:
- 确定PIK3C3对于Shigella flexneri细胞间传播至关重要,在抑制后减少感染焦点大小.
- 需要PIK3C3才能有效地将VLP分解为DMV,包括PtdIns(3) P积累和Dynamin 2招募.
- 抑制PIK3C3也影响了Listeria monocytogenes的传播,特别是在真空细胞逃逸阶段.
结论:
- 在Shigella flexneri传播中,PIK3C3发挥着关键作用,通过PtdIns(3) P和Dynamin 2.P,促进VLP通过PtdIns(3) P和Dynamin 2.P成长为DMV.
- 抑制PIK3C3有效地减少了Shigella flexneri在细胞和动物模型中的传播.
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