한빛사논문
- 조회81
Minjae Kang1†, Min Jeong Kim1†, Dokyung Jeong1, Hyung-Jun Lim1, Ga-eun Go1, Uidon Jeong1, Eunyoung Moon2, Hee-Seok Kweon2, Nae-Gyu Kang3, Seung Jin Hwang3, Sung Hun Youn3, Bo Kyoung Hwang3 and Doory Kim1,4,5,6*
1Department of Chemistry, Hanyang University, Seoul 04763, Republic of Korea
2Electron Microscopy Research Center, Korea Basic Science Institute, Cheongju 28119, Republic of Korea
3R&D Center, LG H&H Co., Ltd, Seoul 07795, Republic of Korea
4Research Institute for Convergence of Basic Science, Hanyang University, Seoul 04763, Republic of Korea
5Institute of Nano Science and Technology, Hanyang University, Seoul 04763, Republic of Korea
6Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Republic of Korea
†Minjae Kang and Min Jeong Kim contributed equally to this work.
*Correspondence: Doory Kim
Abstract
Background: 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).
Results: 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.
Conclusions: 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.
논문정보
- Research article
- 2024년 09월 (BRIC 등록일 2024-09-09)
- 국내 연구진
- 바이오·의료융합 > 바이오·의료융합 기타
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