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渗透压重塑的胶原亚型主导细菌-宿主黏附。

Bacterial-host adhesion dominated by collagen subtypes remodelled by osmotic pressure.

机构信息

Department of Mechanics and Engineering Science, College of Engineering, Peking University, Beijing, China.

State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.

出版信息

NPJ Biofilms Microbiomes. 2024 Nov 12;10(1):124. doi: 10.1038/s41522-024-00600-x.

DOI:10.1038/s41522-024-00600-x
PMID:39532878
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11557999/
Abstract

Environmental osmolarity plays a crucial role in regulating the functions and behaviors of both host cells and pathogens. However, it remains unclear whether and how environmental osmotic stimuli modulate bacterial‒host interfacial adhesion. Using single-cell force spectroscopy, we revealed that the interfacial adhesion force depended nonlinearly on the osmotic prestimulation of host cells but not bacteria. Quantitatively, the adhesion force increased dramatically from 25.98 nN under isotonic conditions to 112.45 or 93.10 nN after the host cells were treated with the hypotonic or hypertonic solution. There was a strong correlation between the adhesion force and the number of host cells harboring adherent/internalized bacteria. We further revealed that enhanced overexpression levels of collagen XV and II were responsible for the increases in interfacial adhesion under hypotonic and hypertonic conditions, respectively. This work provides new opportunities for developing host-directed antibacterial strategies related to interfacial adhesion from a mechanobiological perspective.

摘要

环境渗透压在调节宿主细胞和病原体的功能和行为方面起着至关重要的作用。然而,目前尚不清楚环境渗透刺激是否以及如何调节细菌-宿主界面粘附。使用单细胞力谱技术,我们揭示了界面粘附力与宿主细胞的渗透压预刺激呈非线性相关,但与细菌无关。定量分析表明,在等渗条件下,粘附力为 25.98nN,而在用低渗或高渗溶液处理宿主细胞后,粘附力分别急剧增加到 112.45 或 93.10nN。粘附力与含有粘附/内化细菌的宿主细胞数量之间存在很强的相关性。我们进一步揭示,在低渗和高渗条件下,胶原 XV 和 II 的过度表达水平增强分别导致界面粘附力的增加。这项工作从机械生物学的角度为开发与界面粘附相关的宿主定向抗菌策略提供了新的机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/f4126a64fe3c/41522_2024_600_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/1e3ef68b42fe/41522_2024_600_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/3b9136352df2/41522_2024_600_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/bd8b5a6b0dd9/41522_2024_600_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/c2916419c4a6/41522_2024_600_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/6a10a4ccb14a/41522_2024_600_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/f4126a64fe3c/41522_2024_600_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/1e3ef68b42fe/41522_2024_600_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/3b9136352df2/41522_2024_600_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/bd8b5a6b0dd9/41522_2024_600_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/c2916419c4a6/41522_2024_600_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/6a10a4ccb14a/41522_2024_600_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5424/11557999/f4126a64fe3c/41522_2024_600_Fig6_HTML.jpg

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本文引用的文献

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Geometric constraint-triggered collagen expression mediates bacterial-host adhesion.几何约束触发胶原表达介导细菌-宿主黏附。
Nat Commun. 2023 Dec 9;14(1):8165. doi: 10.1038/s41467-023-43827-6.
2
Autoinducer-2 promotes adherence of through facilitating the expression of MSHA type IV pili genes mediated by c-di-GMP.群体感应信号分子 2 通过促进 c-di-GMP 介导的 MSHA 型 IV 菌毛基因的表达促进 的黏附。
Appl Environ Microbiol. 2023 Nov 29;89(11):e0081923. doi: 10.1128/aem.00819-23. Epub 2023 Oct 30.
3
Response mechanisms to acid stress promote LF82 replication in macrophages.
酸应激反应机制促进巨噬细胞中 LF82 的复制。
Front Cell Infect Microbiol. 2023 Oct 10;13:1255083. doi: 10.3389/fcimb.2023.1255083. eCollection 2023.
4
Catch Bond-Mediated Adhesion Drives Host Cell Invasion.黏附连接介导的捕获驱动宿主细胞入侵。
Nano Lett. 2023 Jun 14;23(11):5297-5306. doi: 10.1021/acs.nanolett.3c01387. Epub 2023 Jun 2.
5
Bacterial defences: mechanisms, evolution and antimicrobial resistance.细菌防御机制:机制、进化和抗微生物药物耐药性。
Nat Rev Microbiol. 2023 Aug;21(8):519-534. doi: 10.1038/s41579-023-00877-3. Epub 2023 Apr 24.
6
Mechanobiological Adaptation to Hyperosmolarity Enhances Barrier Function in Human Vascular Microphysiological System.高渗环境下的机械生物学适应增强了人血管微生理系统的屏障功能。
Adv Sci (Weinh). 2023 May;10(13):e2206384. doi: 10.1002/advs.202206384. Epub 2023 Feb 19.
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Staphylococcus aureus host interactions and adaptation.金黄色葡萄球菌宿主相互作用和适应。
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