Complement-mediated killing of <i>Escherichia coli</i> by mechanical destabilization of the cell envelope

Data for research published as preprint in https://doi.org/10.1101/2023.12.10.570986 and as peer-reviewed paper in Benn, Bortolini et al., EMBO Journal (2024) 43: 6152 - 6160, http://dx.doi.org/10.1038/s44318-024-00266-3, with data here grouped by main figures as in the submitted manuscript.Complement proteins eliminate Gram-negative bacteria in the blood via the formation of membrane attack complex (MAC) pores in the outer membrane. However, it remains unclear how outer membrane poration leads to inner membrane permeation and cell lysis. Using atomic force microscopy (AFM) on living <i>Escherichia coli</i> (<i>E. coli</i>), we probed MAC-induced changes in the cell envelope and correlated these with subsequent cell death. Initially, bacteria survived despite the formation of hundreds of MACs randomly distributed over the cell surface. This was followed by larger-scale disruption of the outer membrane, including propagating defects and fractures, and by an overall swelling and stiffening of the bacterial surface, which precede inner membrane permeation. We conclude that bacterial cell lysis is only an indirect effect of MAC formation; outer membrane poration leads to mechanical destabilization of the cell envelope, reducing its ability to contain the turgor pressure, leading to inner membrane permeation and cell death.The data stored here include AFM data of living <i>E. coli</i> cells exposed to complement proteins and particularly the membrane attack complex; results of data processing in the form of background subtracted images and mechanical data; and brightfield and fluorescence microscopy images that were taken complementary to AFM data on the same cells.Data files can be open with open-source AFM image processing software (e.g., Gwyddion), general image viewers (e.g., for jpeg, tiff, pdf) or any spreadsheet text readers (for e.g. txt and csv files).

本数据集关联的研究成果以预印本形式发布于https://doi.org/10.1101/2023.12.10.570986，并以同行评议论文形式发表于Benn、Bortolini等学者所在的《EMBO Journal》2024年第43卷第6152-6160页，对应DOI为http://dx.doi.org/10.1038/s44318-024-00266-3；本数据集的数据按投稿手稿中的主图进行分组整理。

补体蛋白可通过在革兰氏阴性菌外膜形成膜攻击复合物（membrane attack complex, MAC）孔道，清除血液中的革兰氏阴性菌，但目前学界仍未明确外膜成孔如何引发内膜通透与细胞裂解。本研究借助原子力显微镜（atomic force microscopy, AFM）对活的大肠埃希氏菌（Escherichia coli, E. coli）开展观测，探究MAC诱导的细胞包膜变化，并将其与后续细胞死亡事件进行关联分析。研究发现，即便细胞表面随机分布了数百个MAC孔道，细菌最初仍可存活；随后出现外膜的大规模破坏，包括缺陷与断裂的扩散，同时细菌表面整体呈现肿胀与变硬的特征，该过程发生于内膜通透之前。本研究得出结论：细菌细胞裂解仅是MAC形成的间接效应；外膜成孔会导致细胞包膜发生机械失稳，降低其维持胞内膨压的能力，最终引发内膜通透与细胞死亡。

本数据集存储的数据包括：经补体蛋白（尤其是膜攻击复合物）处理的活大肠埃希氏菌的AFM数据；经背景扣除处理的图像与力学数据等加工后结果；以及与同一观测细胞的AFM数据配套获取的明场与荧光显微镜图像。

数据文件可通过开源AFM图像处理软件（如Gwyddion）、通用图像查看器（如支持jpeg、tiff、pdf格式的工具），或任意文本/电子表格阅读器（如用于读取txt、csv文件的工具）打开读取。

搜集汇总

背景与挑战

背景概述

该数据集聚焦于补体系统通过膜攻击复合物（MAC）对大肠杆菌细胞包膜的机械破坏作用，使用原子力显微镜（AFM）和显微镜图像探究了MAC导致细胞死亡的机制。数据包括AFM原始数据、处理后的图像和力学测量结果，支持相关预印本和已发表论文的研究，适用于细菌学、生物物理学和免疫学领域的分析。文件格式兼容AFM处理软件、图像查看器和文本编辑器，便于科研人员使用。