Deep sequencing-based expression transcriptional profiling changes during Brucella infection

被引:7
作者
Liu, Qianhong [1 ]
Han, Wenyu [1 ]
Sun, Changjiang [1 ]
Zhou, Liang [1 ]
Ma, Limin [1 ]
Lei, Liancheng [1 ]
Yan, Shouqing [1 ]
Liu, Shanshan [1 ]
Du, Chongtao [1 ]
Feng, Xin [1 ]
机构
[1] Jilin Univ, Coll Anim Sci & Vet Med, Changchun 130062, Peoples R China
关键词
Deep sequencing-based expression; Transcription; Infection; Brucella; GENE-EXPRESSION; MD-2; EXPRESSION; ABORTUS; MELITENSIS; PROTEIN; MACROPHAGES; PHAGOCYTOSIS; TRAFFICKING; MUTAGENESIS; RECEPTOR-2;
D O I
10.1016/j.micpath.2012.02.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:267 / 277
页数:11
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