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布鲁氏菌属内病原体感染 HeLa 细胞后的转录谱。

Transcriptional profile of the intracellular pathogen Brucella melitensis following HeLa cells infection.

机构信息

Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, TX, United States.

出版信息

Microb Pathog. 2011 Nov;51(5):338-44. doi: 10.1016/j.micpath.2011.07.006. Epub 2011 Jul 20.

DOI:10.1016/j.micpath.2011.07.006
PMID:21798337
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3170451/
Abstract

Brucella spp. infect hosts primarily by adhering and penetrating mucosal surfaces; however the initial molecular phenomena of this host:pathogen interaction remain poorly understood. Using cDNA microarray analysis, we characterized the transcriptional profile of the intracellular pathogen Brucella melitensis at 4 h (adaptational period) and 12 h (replicative phase) following HeLa cells infection. The intracellular pathogen transcriptome was determined using initially enriched and then amplified B. melitensis RNA from total RNA of B. melitensis-infected HeLa cells. Analysis of microarray results identified 161 and 115 pathogen genes differentially expressed at 4 and 12 h p.i., respectively. In concordance with phenotypic studies, most of the genes expressed were involved in pathogen growth and metabolism, and were down-regulated at the earliest time point (78%), but up-regulated at 12 h p.i. (75%). Further characterization of specific genes identified in this study will elucidate biological processes and pathways to help understand how both host and Brucella interact during the early infectious process to the eventual benefit of the pathogen and to the detriment of the naïve host.

摘要

布鲁氏菌属主要通过黏附和穿透黏膜表面感染宿主; 然而,这种宿主与病原体相互作用的初始分子现象仍知之甚少。我们使用 cDNA 微阵列分析,在 HeLa 细胞感染后 4 小时(适应期)和 12 小时(复制期),对细胞内病原体布鲁氏菌 melitensis 的转录谱进行了描述。使用最初从布鲁氏菌 melitensis 感染的 HeLa 细胞的总 RNA 中富集和扩增的布鲁氏菌 melitensis RNA 来确定细胞内病原体转录组。微阵列结果分析鉴定了 161 个和 115 个病原体基因,分别在 4 和 12 h p.i. 时差异表达。与表型研究一致,大多数表达的基因与病原体的生长和代谢有关,在最早的时间点(78%)下调,但在 12 h p.i.(75%)上调。对本研究中鉴定的特定基因的进一步表征将阐明生物学过程和途径,以帮助理解宿主和布鲁氏菌在早期感染过程中如何相互作用,最终有利于病原体,而不利于幼稚的宿主。

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Occurrence and repair of alkylating stress in the intracellular pathogen Brucella abortus.胞内病原体布鲁氏菌中烷化应激的发生和修复。
Nat Commun. 2019 Oct 24;10(1):4847. doi: 10.1038/s41467-019-12516-8.
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Systems Biology Analysis of Temporal and Bovine Transcriptomes Predicts host:Pathogen Protein-Protein Interactions.时间和牛转录组的系统生物学分析预测宿主:病原体蛋白质-蛋白质相互作用。
Front Microbiol. 2017 Jul 27;8:1275. doi: 10.3389/fmicb.2017.01275. eCollection 2017.
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The invA gene of Brucella melitensis is involved in intracellular invasion and is required to establish infection in a mouse model.羊种布鲁氏菌的invA基因参与细胞内侵袭,是在小鼠模型中建立感染所必需的。
Virulence. 2014 May 15;5(4):563-74. doi: 10.4161/viru.28589. Epub 2014 Mar 25.
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Host-Brucella interactions and the Brucella genome as tools for subunit antigen discovery and immunization against brucellosis.宿主-布鲁氏菌相互作用和布鲁氏菌基因组作为亚单位抗原发现和抗布鲁氏菌病免疫的工具。
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本文引用的文献

1
Selective amplification of Brucella melitensis mRNA from a mixed host-pathogen total RNA.从混合的宿主-病原体总RNA中选择性扩增布鲁氏菌mRNA。
BMC Res Notes. 2010 Sep 28;3:244. doi: 10.1186/1756-0500-3-244.
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Brucella melitensis global gene expression study provides novel information on growth phase-specific gene regulation with potential insights for understanding Brucella:host initial interactions.羊种布鲁氏菌全基因组表达研究提供了关于生长阶段特异性基因调控的新信息,对理解布鲁氏菌与宿主的初始相互作用具有潜在的启示。
BMC Microbiol. 2009 May 6;9:81. doi: 10.1186/1471-2180-9-81.
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Intracellular adaptation of Brucella abortus.流产布鲁氏菌的细胞内适应性
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The BMEI0216 gene of Brucella melitensis is required for internalization in HeLa cells.羊种布鲁氏菌的BMEI0216基因是其在HeLa细胞内化过程所必需的。
Microb Pathog. 2008 Jan;44(1):28-33. doi: 10.1016/j.micpath.2007.08.008. Epub 2007 Aug 14.
5
Brucella suis urease encoded by ure1 but not ure2 is necessary for intestinal infection of BALB/c mice.由ure1而非ure2编码的猪布鲁氏菌脲酶对于BALB/c小鼠的肠道感染是必需的。
BMC Microbiol. 2007 Jun 19;7:57. doi: 10.1186/1471-2180-7-57.
6
Characterization of the urease operon of Brucella abortus and assessment of its role in virulence of the bacterium.流产布鲁氏菌脲酶操纵子的特性及其在细菌毒力中作用的评估。
Infect Immun. 2007 Feb;75(2):774-80. doi: 10.1128/IAI.01244-06. Epub 2006 Nov 13.
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Virulence strategies for infecting phagocytes deduced from the in vivo transcriptional program of Legionella pneumophila.从嗜肺军团菌的体内转录程序推导得出的感染吞噬细胞的毒力策略。
Cell Microbiol. 2006 Aug;8(8):1228-40. doi: 10.1111/j.1462-5822.2006.00703.x.
8
Characterization of SP41, a surface protein of Brucella associated with adherence and invasion of host epithelial cells.布鲁氏菌表面蛋白SP41的特性研究,该蛋白与宿主上皮细胞的黏附和侵袭相关
Cell Microbiol. 2006 Dec;8(12):1877-87. doi: 10.1111/j.1462-5822.2006.00754.x. Epub 2006 Jul 4.
9
The AcrAB-TolC efflux system of Salmonella enterica serovar Typhimurium plays a role in pathogenesis.肠炎沙门氏菌鼠伤寒血清型的AcrAB-TolC外排系统在发病机制中起作用。
Cell Microbiol. 2006 May;8(5):847-56. doi: 10.1111/j.1462-5822.2005.00671.x.
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MotD of Sinorhizobium meliloti and related alpha-proteobacteria is the flagellar-hook-length regulator and therefore reassigned as FliK.苜蓿中华根瘤菌及相关α-变形菌的MotD是鞭毛钩长度调节蛋白,因此重新命名为FliK。
J Bacteriol. 2006 Mar;188(6):2144-53. doi: 10.1128/JB.188.6.2144-2153.2006.