Deep sequencing-based expression transcriptional profiling changes during Brucella infection

Deep sequencing-based expression transcriptional profiling changes during Brucella infection
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布鲁氏菌感染期间基于深度测序的表达转录谱变化

DOI:
10.1016/j.micpath.2012.02.001
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发表时间:
2012-05-01
影响因子:
3.8
通讯作者:
Feng, Xin
Feng, Xin
中科院分区:
医学3区
文献类型:
--
作者:
Liu, Qianhong;Han, Wenyu;Feng, Xin

文献摘要

被引文献

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布鲁氏菌病是一种世界性的人畜共患传染病,对畜牧业生产和人类健康具有重大的经济影响。宿主巨噬细胞-布鲁氏菌相互作用对感染的建立至关重要。因此,在本研究中使用基于深度测序的技术研究了感染羊种布鲁氏菌菌株16 M的巨噬细胞中基因表达的动力学转录谱。感染后0、4和24 h从巨噬细胞中提取总RNA。数据分析表明,在基因本体论术语,在内质网,溶酶体,以及那些参与程序性细胞死亡和凋亡的基因的表达显着变化,在感染后的第一个24小时。途径富集分析表明,凋亡途径中的基因。NOD样受体信号通路、Fc γ R介导的吞噬作用、溶酶体通路、p53信号通路和内质网中的蛋白加工在感染后的前24 h内显著改变。与感染后4 h相比,感染后24 h B细胞受体和Toll样受体信号通路也发生了显著变化。本研究的结果有助于更好地理解宿主细胞反应的方式,以防止布鲁氏菌感染。(c)2012爱思唯尔有限公司保留所有权利。
Brucellosis is a worldwide zoonotic infectious disease that has significant economic effects on animal production and human health. The host macrophage - Brucella interaction is critical to the establishment of infections. Thus, the kinetic transcriptional profile of gene expression in macrophages infected with the Brucella melitensis strain 16M was investigated in the current study using a technology based on deep sequencing. The total RNA was extracted from macrophages 0, 4, and 24 h post-infection. Data analysis showed that in the gene ontology term, the expression of genes in the endoplasmic reticulum, lysosomes, as well as those involved in programmed cell death and apoptosis significantly changed during the first 24 h post-infection. Pathway enrichment analysis indicated that the genes in the apoptosis pathway. NOD-like receptor signaling pathway, Fc gamma R-mediated phagocytosis, lysosome pathway, p53 signaling pathway, and protein processing in the endoplasmic reticulum significantly changed during the first 24 h post-infection. The B-cell receptor and toll-like receptor signaling pathways were also significantly changed 24 h post-infection compared with those 4 h post-infection. The results of the current study can contribute to an improved understanding of the manner by which host cell responses may be manipulated to prevent Brucella infection. (c) 2012 Elsevier Ltd. All rights reserved.