Japanese encephalitis virus infection induces changes of mRNA profile of mouse spleen and brain

被引:46
作者
Yang, Yang [1 ,2 ]
Ye, Jing [1 ,2 ]
Yang, Xiaohong [1 ,2 ]
Jiang, Rong [1 ,2 ]
Chen, Huanchun [1 ,2 ]
Cao, Shengbo [1 ,2 ]
机构
[1] Huazhong Agr Univ, State Key Lab Agr Microbiol, Wuhan 430070, Peoples R China
[2] Huazhong Agr Univ, Coll Vet Med, Lab Anim Virol, Wuhan 430070, Peoples R China
关键词
WEST-NILE-VIRUS; PERIVASCULAR MACROPHAGES; GENE-EXPRESSION; DENGUE VIRUS; GRANZYME-B; CELL-DEATH; INFLAMMATION; SUSCEPTIBILITY; INTERLEUKIN-6; ACTIVATION;
D O I
10.1186/1743-422X-8-80
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Background: Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus, leading to an acute encephalitis and damage to the central nervous system (CNS). The mechanism of JEV pathogenesis is still unclear. DNA microarray analyses have been recently employed to detect changes in host gene expression, which is helpful to reveal molecular pathways that govern viral pathogenesis. In order to globally identify candidate host genes associated with JEV pathogenesis, a systematic mRNA profiling was performed in spleens and brains of JEV-infected mice. Results: The results of microarray analysis showed that 437 genes in spleen and 1119 genes in brain were differentially expressed in response to JEV infection, with obviously upregulated genes like pro-inflammatory chemokines and cytokines, apoptosis-related proteases and IFN inducible transcription factors. And the significant pathways of differentially expressed genes are involved in cytokine-cytokine receptor interaction, natural killer cell mediated cytotoxicity, antigen processing and presentation, MAPK signaling, and toll-like receptor signaling, etc. The differential expression of these genes suggests a strong antiviral response of host but may also contribute to the pathogenesis of JEV resulting in encephalitis. Quantitative RT-PCR (RT-qPCR) assay of some selected genes further confirmed the results of microarray assay. Conclusions: Data obtained from mRNA microarray suggests that JEV infection causes significant changes of mRNA expression profiles in mouse spleen and brain. Most of differentially expression genes are associated with antiviral response of host, which may provide important information for investigation of JEV pathogenesis and therapeutic method.
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页数:11
相关论文
共 36 条
[1]   Functional Modulation of Dendritic Cells and Macrophages by Japanese Encephalitis Virus through MyD88 Adaptor Molecule-Dependent and -Independent Pathways [J].
Aleyas, Abi G. ;
George, Junu A. ;
Han, Young Woo ;
Rahman, M. M. ;
Kim, Seon Ju ;
Han, Sang Bae ;
Kim, Byung Sam ;
Kim, Koanhoi ;
Eo, Seong Kug .
JOURNAL OF IMMUNOLOGY, 2009, 183 (04) :2462-2474
[2]   Immunomodulatory Cytokines Determine the Outcome of Japanese Encephalitis Virus Infection in Mice [J].
Biswas, S. M. ;
Kar, S. ;
Singh, R. ;
Chakraborty, D. ;
Vipat, V. ;
Raut, C. G. ;
Mishra, A. C. ;
Gore, M. M. ;
Ghosh, D. .
JOURNAL OF MEDICAL VIROLOGY, 2010, 82 (02) :304-310
[3]   CD163, a marker of perivascular macrophages, is up-regulated by microglia in simian immunodeficiency virus encephalitis after haptoglobin-hemoglobin complex stimulation and is suggestive of breakdown of the blood-brain barrier [J].
Borda, Juan T. ;
Alvarez, Xavier ;
Mohan, Mahesh ;
Hasegawa, Atsuhiko ;
Bernardino, Andrea ;
Jean, Sherrie ;
Aye, Pyone ;
Lackner, Andrew A. .
AMERICAN JOURNAL OF PATHOLOGY, 2008, 172 (03) :725-737
[4]  
Browne KA, 1999, MOL CELL BIOL, V19, P8604
[5]   Circulating interleukin-6 mediates the febrile response to localised inflammation in rats [J].
Cartmell, T ;
Poole, S ;
Turnbull, AV ;
Rothwell, NJ ;
Luheshi, GN .
JOURNAL OF PHYSIOLOGY-LONDON, 2000, 526 (03) :653-661
[6]   Flavivirus induces interferon-beta gene expression through a pathway involving RIG-I-dependent IRF-3 and PI3K-dependent NF-κB activation [J].
Chang, TH ;
Liao, CL ;
Lin, YL .
MICROBES AND INFECTION, 2006, 8 (01) :157-171
[7]   The host response to West Nile Virus infection limits viral spread through the activation of the interferon regulatory factor 3 pathway [J].
Fredericksen, BL ;
Smith, M ;
Katze, MG ;
Shi, PY ;
Gale, M .
JOURNAL OF VIROLOGY, 2004, 78 (14) :7737-7747
[8]   Chemokine profiling of Japanese encephalitis virus-infected mouse neuroblastoma cells by microarray and real-time RT-PCR: Implication in neuropathogenesis [J].
Gupta, Nimesh ;
Santhosh, S. R. ;
Babu, J. Pradeep ;
Parida, M. M. ;
Rao, P. V. Lakshmana .
VIRUS RESEARCH, 2010, 147 (01) :107-112
[9]   An outbreak of Japanese encephalitis in the Torres Strait, Australia, 1995 [J].
Hanna, JN ;
Ritchie, SA ;
Phillips, DA ;
Shield, J ;
Bailey, MC ;
Mackenzie, JS ;
Poidinger, M ;
McCall, BJ ;
Mills, PJ .
MEDICAL JOURNAL OF AUSTRALIA, 1996, 165 (05) :256-260
[10]   The chemokines CXCL9 and CXCL10 promote a protective immune response but do not contribute to cardiac inflammation following infection with Trypanosoma cruzi [J].
Hardison, JL ;
Wrightsman, RA ;
Carpenter, PM ;
Lane, TE ;
Manning, JE .
INFECTION AND IMMUNITY, 2006, 74 (01) :125-134