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脂质巨泡通过轻微增强细胞膜流动性吞噬活细菌。

Lipid Giant Vesicles Engulf Living Bacteria Triggered by Minor Enhancement in Membrane Fluidity.

机构信息

CAS Key Laboratory of Colloid, Interface and Chemical Thermodynamics, CAS Research/Education Center for Excellence in Molecular Sciences, Beijing National Laboratory for Molecular Sciences, Institute of Chemistry, Chinese Academy of Sciences, Beijing 100190, China.

University of Chinese Academy of Sciences, Beijing 100049, China.

出版信息

Nano Lett. 2023 Jan 11;23(1):371-379. doi: 10.1021/acs.nanolett.2c03475. Epub 2022 Nov 28.

Abstract

Antibacterial amphiphiles normally kill bacteria by destroying the bacterial membrane. Whether and how antibacterial amphiphiles alter normal cell membrane and lead to subsequent effects on pathogen invasion into cells have been scarcely promulgated. Herein, by taking four antibacterial gemini amphiphiles with different spacer groups to modulate cell-mimic phospholipid giant unilamellar vesicles (GUVs), bacteria adhesion on the modified GUVs surface and bacteria engulfment process by the GUVs are clearly captured by confocal laser scanning microscopy. Further characterization shows that the enhanced cationic surface charge of GUVs by the amphiphiles determines the bacteria adhesion amount, while the involvement of amphiphile in GUVs results in looser molecular arrangement and concomitant higher fluidity in the bilayer membranes, facilitating the bacteria intruding into GUVs. This study sheds new light on the effect of amphiphiles on membrane bilayer and the concurrent effect on pathogen invasion into cell mimics and broadens the nonprotein-mediated endocytosis pathway for live bacteria.

摘要

抗菌两亲分子通常通过破坏细菌膜来杀死细菌。抗菌两亲分子是否以及如何改变正常细胞膜,并对随后的病原体入侵细胞产生影响,尚未得到充分阐明。在此,通过采用具有不同间隔基的四种抗菌双子型两亲分子来调节细胞模拟磷脂巨大单层囊泡(GUVs),利用共聚焦激光扫描显微镜清楚地捕捉到了修饰后的 GUVs 表面上的细菌黏附以及 GUVs 吞噬细菌的过程。进一步的表征表明,两亲分子增强了 GUVs 的阳离子表面电荷,决定了细菌的黏附量,而两亲分子的参与导致双层膜中分子排列更加松散,伴随更高的流动性,从而有利于细菌侵入 GUVs。本研究揭示了两亲分子对膜双层的作用以及对病原体入侵细胞模拟物的并发作用,拓宽了活细菌的非蛋白介导内吞途径。

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