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细胞骨架作为炭疽毒素的一个新兴靶标。

Cytoskeleton as an emerging target of anthrax toxins.

机构信息

Unité Interactions Hôte-Agents pathogènes, Institut de Recherche Biomédicale des Armées, Centre de Recherche du Service de Santé des Armées, BP 87, 24 avenue des Maquis du Grésivaudan 38702 La Tronche Cedex, France.

出版信息

Toxins (Basel). 2012 Feb;4(2):83-97. doi: 10.3390/toxins4020083. Epub 2012 Feb 6.

DOI:10.3390/toxins4020083
PMID:22474568
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3317109/
Abstract

Bacillus anthracis, the agent of anthrax, has gained virulence through its exotoxins produced by vegetative bacilli and is composed of three components forming lethal toxin (LT) and edema toxin (ET). So far, little is known about the effects of these toxins on the eukaryotic cytoskeleton. Here, we provide an overview on the general effects of toxin upon the cytoskeleton architecture. Thus, we shall discuss how anthrax toxins interact with their receptors and may disrupt the interface between extracellular matrix and the cytoskeleton. We then analyze what toxin molecular effects on cytoskeleton have been described, before discussing how the cytoskeleton may help the pathogen to corrupt general cell processes such as phagocytosis or vascular integrity.

摘要

炭疽杆菌是炭疽的病原体,通过其营养体产生的外毒素获得了毒力,由形成致死毒素 (LT) 和水肿毒素 (ET) 的三个成分组成。到目前为止,人们对这些毒素对真核细胞骨架的影响知之甚少。在这里,我们提供了一个关于毒素对细胞骨架结构的一般影响的概述。因此,我们将讨论炭疽毒素如何与其受体相互作用,并可能破坏细胞外基质与细胞骨架之间的界面。然后,我们分析了已经描述的毒素对细胞骨架的分子作用,接着讨论了细胞骨架如何帮助病原体破坏吞噬作用或血管完整性等一般细胞过程。

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本文引用的文献

1
cAMP signaling by anthrax edema toxin induces transendothelial cell tunnels, which are resealed by MIM via Arp2/3-driven actin polymerization.炭疽毒素通过 cAMP 信号诱导细胞间隧道形成,该隧道通过肌球蛋白轻链激酶(MIM)通过 Arp2/3 驱动的肌动蛋白聚合作用重新封闭。
Cell Host Microbe. 2011 Nov 17;10(5):464-74. doi: 10.1016/j.chom.2011.09.014.
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Anthrax lethal toxin-mediated disruption of endothelial VE-cadherin is attenuated by inhibition of the Rho-associated kinase pathway.炭疽致死毒素介导的内皮 VE-cadherin 破坏被 Rho 相关激酶途径抑制所减弱。
Toxins (Basel). 2011 Oct;3(10):1278-93. doi: 10.3390/toxins3101278. Epub 2011 Oct 20.
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酿酒酵母CNCM I-745菌株对炭疽杆菌致死毒素具有保护作用。
Toxins (Basel). 2015 Oct 30;7(11):4455-67. doi: 10.3390/toxins7114455.
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Micropatterned macrophage analysis reveals global cytoskeleton constraints induced by Bacillus anthracis edema toxin.微图案巨噬细胞分析揭示炭疽杆菌水肿毒素诱导的整体细胞骨架限制。
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Regulatory mechanisms of anthrax toxin receptor 1-dependent vascular and connective tissue homeostasis.炭疽毒素受体1依赖性血管和结缔组织稳态的调节机制。
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Bacillus anthracis cell wall peptidoglycan but not lethal or edema toxins produces changes consistent with disseminated intravascular coagulation in a rat model.炭疽杆菌细胞壁肽聚糖而非致死或水肿毒素在大鼠模型中产生与弥散性血管内凝血一致的变化。
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Anthrax lethal toxin downregulates claudin-5 expression in human endothelial tight junctions.炭疽致死毒素下调人内皮紧密连接中的紧密连接蛋白-5 的表达。
PLoS One. 2013 Apr 23;8(4):e62576. doi: 10.1371/journal.pone.0062576. Print 2013.
8
Studies in mice reveal a role for anthrax toxin receptors in matrix metalloproteinase function and extracellular matrix homeostasis.在小鼠中的研究揭示了炭疽毒素受体在基质金属蛋白酶功能和细胞外基质动态平衡中的作用。
Toxins (Basel). 2013 Feb 6;5(2):315-26. doi: 10.3390/toxins5020315.
Emergence of anthrax edema toxin as a master manipulator of macrophage and B cell functions.
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Microbes Infect. 2012 Feb;14(2):97-118. doi: 10.1016/j.micinf.2011.08.016. Epub 2011 Sep 8.
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