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体外感染低致病性禽流感病毒后原代鸡细胞培养中的转录因子调控和细胞因子表达。

Transcription factor regulation and cytokine expression following in vitro infection of primary chicken cell culture with low pathogenic avian influenza virus.

机构信息

Exotic and Emerging Avian Disease Research Unit, Southeast Poultry Research Laboratory, Agricultural Research Service, USDA, 934 College Station Road, Athens, GA 30605, Greece.

出版信息

Virol J. 2013 Nov 19;10:342. doi: 10.1186/1743-422X-10-342.

Abstract

BACKGROUND

Avian influenza virus (AIV) induced proinflammatory cytokine expression is believed to contribute to the disease pathogenesis following infection of poultry. However, there is limited information on the avian immune response to infection with low pathogenic avian influenza virus (LPAIV).

METHODS

To gain a better understanding of the early viral-host interactions of LPAIV in chickens, primary chicken embryo hepatocytes (CEH) were infected with four different LPAIVs of U.S. origin. Kinetics of virus replication, transcription factor (c-Jun, p50 and IRF-3) activation and immune response gene (IL-6, IL-1beta, IFN-alpha and Mx) expression were studied at four different time points (6, 12, 24 and 48 hours) post infection and compared to non-infected controls.

RESULTS

CEH can support growth of the tested LPAIVs when with trypsin supplementation. All four immune response genes tested were upregulated following infection as were transcription factors c-Jun, p50 and IRF-3. Amplification of these genes was dependant on virus replication (e.g. inclusion of trypsin), such that immune response genes and transcription factors were upregulated as viral titers increased.

CONCLUSION

The results of these studies demonstrate the requirement of virus replication for innate immune regulation and broaden our understanding of transcription factor responses related to LPAIV infection in chickens.

摘要

背景

据信,禽流感病毒(AIV)诱导的促炎细胞因子表达有助于禽类感染后的疾病发病机制。然而,对于低致病性禽流感病毒(LPAIV)感染后禽类的免疫反应,信息有限。

方法

为了更好地了解 LPAIV 在鸡体内的早期病毒-宿主相互作用,用来自美国的四种不同的 LPAIV 感染原代鸡胚肝细胞(CEH)。在感染后四个不同时间点(6、12、24 和 48 小时)研究病毒复制、转录因子(c-Jun、p50 和 IRF-3)激活和免疫反应基因(IL-6、IL-1β、IFN-α和 Mx)表达的动力学,并与未感染对照进行比较。

结果

在添加胰蛋白酶的情况下,CEH 可以支持测试的 LPAIV 的生长。四种测试的免疫反应基因均在感染后上调,转录因子 c-Jun、p50 和 IRF-3 也是如此。这些基因的扩增依赖于病毒复制(例如,包含胰蛋白酶),因此随着病毒滴度的增加,免疫反应基因和转录因子被上调。

结论

这些研究的结果表明,固有免疫调节需要病毒复制,并拓宽了我们对与鸡感染 LPAIV 相关的转录因子反应的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/870e/4225510/1c3a28e8f7db/1743-422X-10-342-1.jpg

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