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Analysis of Shigella flexneri Resistance, Biofilm Formation, and Transcriptional Profile in Response to Bile Salts.福氏志贺菌对胆盐的耐药性、生物膜形成及转录谱分析
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The actin-based motility defect of a Shigella flexneri rmlD rough LPS mutant is not due to loss of IcsA polarity.弗氏志贺氏菌rmlD粗糙脂多糖突变体基于肌动蛋白的运动缺陷并非由于IcsA极性丧失所致。
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Mutagenesis of the Shigella flexneri autotransporter IcsA reveals novel functional regions involved in IcsA biogenesis and recruitment of host neural Wiscott-Aldrich syndrome protein.福氏志贺菌自转运蛋白IcsA的诱变揭示了参与IcsA生物合成和宿主神经维斯科特-奥尔德里奇综合征蛋白募集的新功能区域。
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Disruption of IcsP, the major Shigella protease that cleaves IcsA, accelerates actin-based motility.IcsP是痢疾杆菌中切割IcsA的主要蛋白酶,IcsP的缺失会加速基于肌动蛋白的运动。
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本文引用的文献

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Interactions between Bacteria and Bile Salts in the Gastrointestinal and Hepatobiliary Tracts.胃肠道和肝胆道中细菌与胆汁盐之间的相互作用
Front Med (Lausanne). 2017 Oct 3;4:163. doi: 10.3389/fmed.2017.00163. eCollection 2017.
2
Autotransporter Adhesins in Escherichia coli Pathogenesis.大肠杆菌发病机制中的自转运黏附素。
Proteomics. 2017 Dec;17(23-24). doi: 10.1002/pmic.201600431. Epub 2017 Oct 12.
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Estimates of global, regional, and national morbidity, mortality, and aetiologies of diarrhoeal diseases: a systematic analysis for the Global Burden of Disease Study 2015.全球、区域和国家腹泻病的发病率、死亡率及病因估计:全球疾病负担研究2015的系统分析
Lancet Infect Dis. 2017 Sep;17(9):909-948. doi: 10.1016/S1473-3099(17)30276-1. Epub 2017 Jun 1.
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How Do the Virulence Factors of Work Together to Cause Disease?[病原体名称]的毒力因子如何共同作用导致疾病?
Front Cell Infect Microbiol. 2017 Mar 24;7:64. doi: 10.3389/fcimb.2017.00064. eCollection 2017.
5
Analysis of Shigella flexneri Resistance, Biofilm Formation, and Transcriptional Profile in Response to Bile Salts.福氏志贺菌对胆盐的耐药性、生物膜形成及转录谱分析
Infect Immun. 2017 May 23;85(6). doi: 10.1128/IAI.01067-16. Print 2017 Jun.
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Identification of Escherichia coli and Shigella Species from Whole-Genome Sequences.从全基因组序列中鉴定大肠杆菌和志贺氏菌属
J Clin Microbiol. 2017 Feb;55(2):616-623. doi: 10.1128/JCM.01790-16. Epub 2016 Dec 14.
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Biofilms: an emergent form of bacterial life.生物膜:细菌的一种新兴生命形式。
Nat Rev Microbiol. 2016 Aug 11;14(9):563-75. doi: 10.1038/nrmicro.2016.94.
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Survival of the Fittest: How Bacterial Pathogens Utilize Bile To Enhance Infection.适者生存:细菌病原体如何利用胆汁增强感染
Clin Microbiol Rev. 2016 Oct;29(4):819-36. doi: 10.1128/CMR.00031-16.
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Bile signalling promotes chronic respiratory infections and antibiotic tolerance.胆汁信号促进慢性呼吸道感染和抗生素耐药性。
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Investigating the Relatedness of Enteroinvasive Escherichia coli to Other E. coli and Shigella Isolates by Using Comparative Genomics.通过比较基因组学研究侵袭性大肠杆菌与其他大肠杆菌和志贺氏菌分离株的相关性。
Infect Immun. 2016 Jul 21;84(8):2362-2371. doi: 10.1128/IAI.00350-16. Print 2016 Aug.

自转运器 IcsA 在胆汁盐存在的情况下促进福氏志贺菌生物膜的形成。

The Autotransporter IcsA Promotes Shigella flexneri Biofilm Formation in the Presence of Bile Salts.

机构信息

Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia, USA.

Department of Biology, University of Puerto Rico at Ponce, Ponce, Puerto Rico, USA.

出版信息

Infect Immun. 2019 Jun 20;87(7). doi: 10.1128/IAI.00861-18. Print 2019 Jul.

DOI:10.1128/IAI.00861-18
PMID:30988059
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6589070/
Abstract

is an intracellular bacterial pathogen that invades epithelial cells in the colonic mucosa, leading to bloody diarrhea. A previous study showed that forms biofilms in the presence of bile salts, through an unknown mechanism. Here, we investigated the potential role of adhesin-like autotransporter proteins in biofilm formation. BLAST search analysis revealed that the 2457T genome harbors 4 genes, , , , and , encoding adhesin-like autotransporter proteins. Deletion mutants of the , , and genes were generated and tested for biofilm formation. Phenotypic analysis of the mutant strains revealed that disruption of abolished bile salt-induced biofilm formation. IcsA is an outer membrane protein secreted at the bacterial pole that is required for actin-based motility during intracellular infection. In extracellular biofilms, IcsA was also secreted at the bacterial pole and mediated bacterial cell-cell contacts and aggregative growth in the presence of bile salts. Dissecting individual roles of bile salts showed that deoxycholate is a robust biofilm inducer compared to cholate. The release of the extracellular domain of IcsA through IcsP-mediated cleavage was greater in the presence of cholate, suggesting that the robustness of biofilm formation was inversely correlated with IcsA processing. Accordingly, deletion of abrogated IcsA processing in biofilms and enhanced biofilm formation.

摘要

是一种细胞内细菌病原体,它会入侵结肠黏膜上皮细胞,导致血性腹泻。先前的研究表明,在胆汁盐存在的情况下,通过未知机制形成生物膜。在这里,我们研究了黏附素样自转运蛋白在生物膜形成中的潜在作用。BLAST 搜索分析表明,2457T 基因组含有编码黏附素样自转运蛋白的 4 个基因、、、和。缺失突变体的、、和基因被生成并测试生物膜形成。突变株的表型分析表明,破坏基因导致胆汁盐诱导的生物膜形成被消除。IcsA 是一种在细菌极部分泌的外膜蛋白,在细胞内感染期间,是肌动蛋白依赖的运动所必需的。在细胞外生物膜中,IcsA 也在细菌极部分泌,并在胆汁盐存在下介导细菌细胞-细胞接触和聚集生长。对胆汁盐的单独作用进行剖析表明,与胆酸钠相比,脱氧胆酸钠是一种更强的生物膜诱导剂。通过 IcsP 介导的切割释放的 IcsA 细胞外结构域在胆酸钠存在下释放更多,这表明生物膜形成的稳健性与 IcsA 加工呈负相关。因此,基因的缺失消除了生物膜中 IcsA 的加工,并增强了生物膜的形成。