Innate immune response to H3N2 and H1N1 influenza virus infection in a human lung organ culture model
Innate immune response to H3N2 and H1N1 influenza virus infection in a human lung organ culture model
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DOI：
10.1016/j.virol.2009.10.016
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发表时间：
2010-01-20
期刊：
影响因子：
3.7
通讯作者：
Metcalf, Jordan P.
中科院分区：
文献类型：
--
作者：
Wu, Wenxin;Booth, J. Leland;Metcalf, Jordan P.
我们在一种新的人肺组织模型中研究了细胞因子对流感病毒PR 8（H1 N1）和俄克拉荷马州/309/06（OK/06，H3 N2）的应答。暴露于流感病毒的模型迅速激活丝裂原活化蛋白激酶信号转导（MAPK）途径ERK，p38和JNK。此外，RNA酶保护试验证实了病毒对几种细胞因子和趋化因子mRNA的诱导作用。这一发现反映在翻译水平，如通过ELISA测定的IL-6、MCP-1、MIP-1 α/β、IL-8和IP-10蛋白被诱导。IP-10和MIP-1 α的免疫组化显示肺泡上皮细胞和巨噬细胞是这两种细胞因子的来源。总之，PR 8和0 K/06在人肺中引起细胞因子的类似诱导，尽管0 K/06在诱导趋化因子MCP-1和IL-8方面不太有效。因此，这种人体器官培养模型应该提供一个相关的平台，研究人肺对流感病毒感染的生物学反应。由爱思唯尔公司出版
We studied cytokine responses to influenza virus PR8 (H1N1) and Oklahoma/309/06 (OK/06, H3N2) in a novel human lung tissue model. Exposure of the model to influenza virus rapidly activated the mitogen-activated protein kinase signaling (MAPK) pathways ERK, p38 and JNK. In addition, RNase protection assay demonstrated the induction of several cytokine and chemokine mRNAs by virus. This finding was reflected at the translational level as IL-6, MCP-1, MIP-1 alpha/beta, IL-8 and IP-10 proteins were induced as determined by ELISA. Immunohistochemistry for IP-10 and MIP-1 alpha revealed that alveolar epithelial cells and macrophages were the source of these two cytokines. Taken together, both PR8 and OK/06 cause similar induction of cytokines in human lung, although OK/06 is less effective at inducing the chemokines MCP-1 and IL-8. This human organ culture model should thus provide a relevant platform to study the biological responses of human lung to influenza virus infection. Published by Elsevier Inc.