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H9N2亚型禽流感病毒感染的BALB/c小鼠肺和脑中NLRP3及其相关细胞因子的表达模式

Expression pattern of NLRP3 and its related cytokines in the lung and brain of avian influenza virus H9N2 infected BALB/c mice.

作者信息

Yu Meng, Zhang Kaizhao, Qi Wenbao, Huang Zhiqiang, Ye Jinhui, Ma Yongjiang, Liao Ming, Ning Zhangyong

机构信息

College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, People's Republic of China.

出版信息

Virol J. 2014 Dec 30;11:229. doi: 10.1186/s12985-014-0229-5.

Abstract

BACKGROUND

H9N2 avian influenza virus (AIV) becomes the focus for its ability of transmission to mammals and as a donor to provide internal genes to form the new epidemic lethal influenza viruses. Residue 627 in PB2 has been proven the virulence factor of H9N2 avian influenza virus in mice, but the detailed data for inflammation difference between H9N2 virus strains with site 627 mutation is still unclear. The inflammasome NLRP3 is recently reported as the cellular machinery responsible for activation of inflammatory processes and plays an important role during the development of inflammation caused by influenza virus infection.

METHODS

In this study, we investigated the expression pattern of NLRP3 and its related cytokines of IL-1β and TNF-α in BALB/c mice infected by H9N2 AIV strains with only a site 627 difference at both mRNA and protein levels at different time points.

RESULTS

The results showed that the expression level of NLRP3, IL-1β and TNF-α changed in the lung and brain of BALB/c mice after infection by VK627 and rVK627E. The immunohistological results showed that the positive cells of NLRP3, IL-1β and TNF-α altered the positive levels of original cells in tissues and infiltrated inflammatory cells which caused by H9N2 infection.

CONCLUSIONS

Our results provided the basic data at differences in expression pattern of NLRP3 and its related cytokines in BALB/c mice infected by H9N2 influenza viruses with only a site 627 difference. This implied that NLRP3 inflammasome plays a role in host response to influenza virus infection and determines the outcome of clinical manifestation and pathological injury. This will explain the variable of pathological presentation in tissues and enhance research on inflammation process of the AIV H9N2 infection.

摘要

背景

H9N2禽流感病毒(AIV)因其向哺乳动物传播的能力以及作为提供内部基因以形成新型致死性流感病毒的供体而成为焦点。PB2蛋白第627位残基已被证明是H9N2禽流感病毒在小鼠中的毒力因子,但关于具有627位点突变的H9N2病毒株之间炎症差异的详细数据仍不清楚。炎性小体NLRP3最近被报道为负责激活炎症过程的细胞机制,并且在流感病毒感染引起的炎症发展过程中起重要作用。

方法

在本研究中,我们调查了仅在第627位点存在差异的H9N2 AIV毒株感染BALB/c小鼠后,在不同时间点NLRP3及其相关细胞因子IL-1β和TNF-α在mRNA和蛋白质水平的表达模式。

结果

结果显示,感染VK627和rVK627E后,BALB/c小鼠肺和脑中NLRP3、IL-1β和TNF-α的表达水平发生变化。免疫组织学结果显示,NLRP3、IL-1β和TNF-α的阳性细胞改变了组织中原始细胞的阳性水平,并浸润了由H9N2感染引起的炎性细胞。

结论

我们的结果提供了仅在第627位点存在差异的H9N2流感病毒感染BALB/c小鼠时NLRP3及其相关细胞因子表达模式差异的基础数据。这表明NLRP3炎性小体在宿主对流感病毒感染的反应中起作用,并决定临床表现和病理损伤的结果。这将解释组织中病理表现的差异,并加强对AIV H9N2感染炎症过程的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cdc/4296676/b3d7e033186b/12985_2014_229_Fig1_HTML.jpg

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