No apoptotic deaths and different levels of inductions of inflammatory cytokines in alveolar macrophages infected with influenza viruses
No apoptotic deaths and different levels of inductions of inflammatory cytokines in alveolar macrophages infected with influenza viruses
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DOI：
10.1016/j.virol.2004.08.019
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发表时间：
2004-11-24
期刊：
影响因子：
3.7
通讯作者：
Webster, RG
中科院分区：
文献类型：
--
作者：
Seo, SH;Webby, R;Webster, RG
据报道，流感病毒主要感染宿主的呼吸道上皮。我们在猪模型中的研究表明，甲型流感病毒感染组成性驻留在呼吸道中的肺泡巨噬细胞，而不会引起细胞凋亡。肿瘤坏死因子α是在这些巨噬细胞中最高度诱导的炎性细胞因子。在体内，人H3 N2流感病毒感染的肺泡巨噬细胞比人H1N1流感病毒感染的肺泡巨噬细胞显示出更高的肿瘤坏死因子α表达。特异性炎性细胞因子如TNF-α的诱导是涉及HA和NA基因的多基因性状。肿瘤坏死因子α表达的显著升高可能是H3 N2流感病毒感染老年患者死亡率高的原因。(C)2004爱思唯尔公司All rights reserved.
Influenza viruses are reported to infect mainly the respiratory tract epithelium of hosts. Our studies in a pig model show that influenza A viruses infect alveolar macrophages that constitutively reside in the respiratory tract, without causing apoptosis. Tumor necrosis factor alpha was the inflammatory cytokine most highly induced in these macrophages. Tit vivo, alveolar macrophages infected with human H3N2 influenza virus showed greater expression of tumor necrosis factor alpha than did alveolar macrophages infected with human H IN I influenza virus. Induction of specific inflammatory cytokine such as TNF-alpha is a polygenic trait that involves the HA and NA genes. Markedly elevated expression of tumor necrosis factor alpha may be responsible for the high mortality rate caused by H3N2 influenza virus infection in elderly patients. (C) 2004 Elsevier Inc. All rights reserved.