Department of Chemistry, Hanyang University, Seoul, 04763, Republic of Korea.
Electron Microscopy Research Center, Korea Basic Science Institute, Cheongju, 28119, Republic of Korea.
J Nanobiotechnology. 2024 Sep 6;22(1):548. doi: 10.1186/s12951-024-02817-6.
Bacterial extracellular vesicles (EVs) are pivotal mediators of intercellular communication and influence host cell biology, thereby contributing to the pathogenesis of infections. Despite their significance, the precise effects of bacterial EVs on the host cells remain poorly understood. This study aimed to elucidate ultrastructural changes in host cells upon infection with EVs derived from a pathogenic bacterium, Staphylococcus aureus (S. aureus).
Using super-resolution fluorescence microscopy and high-voltage electron microscopy, we investigated the nanoscale alterations in mitochondria, endoplasmic reticulum (ER), Golgi apparatus, lysosomes, and microtubules of skin cells infected with bacterial EVs. Our results revealed significant mitochondrial fission, loss of cristae, transformation of the ER from tubular to sheet-like structures, and fragmentation of the Golgi apparatus in cells infected with S. aureus EVs, in contrast to the negligible effects observed following S. epidermidis EV infection, probably due to the pathogenic factors in S. aureus EV, including protein A and enterotoxin. These findings indicate that bacterial EVs, particularly those from pathogenic strains, induce profound ultrastructural changes of host cells that can disrupt cellular homeostasis and contribute to infection pathogenesis.
This study advances the understanding of bacterial EV-host cell interactions and contributes to the development of new diagnostic and therapeutic strategies for bacterial infections.
细菌细胞外囊泡（EVs）是细胞间通讯的关键介质，影响宿主细胞生物学，从而有助于感染的发病机制。尽管它们意义重大，但细菌 EV 对宿主细胞的确切影响仍知之甚少。本研究旨在阐明感染源自致病性细菌金黄色葡萄球菌（S. aureus）的 EV 后宿主细胞的超微结构变化。
使用超分辨率荧光显微镜和高压电子显微镜，我们研究了感染细菌 EV 的皮肤细胞中线粒体、内质网（ER）、高尔基体、溶酶体和微管的纳米级变化。我们的结果显示，与 S. epidermidis EV 感染相比，感染 S. aureus EV 的细胞中线粒体明显分裂、嵴丢失、ER 从管状转变为片状结构以及高尔基体碎片化，这可能是由于 S. aureus EV 中的致病因子，包括蛋白 A 和肠毒素所致。这些发现表明，细菌 EV，特别是来自致病性菌株的 EV，会引起宿主细胞的深刻超微结构变化，从而破坏细胞内稳态并有助于感染发病机制。
本研究增进了对细菌 EV-宿主细胞相互作用的理解，并为细菌感染的新诊断和治疗策略的发展做出了贡献。
