Bussfeld D, Kaufmann A, Meyer R G, Gemsa D, Sprenger H
Institute of Immunology, Philipps-University, Marburg, Germany.
Cell Immunol. 1998 May 25;186(1):1-7. doi: 10.1006/cimm.1998.1295.
After influenza A virus infection of human monocytes, we found a rapid and marked release of the mononuclear cell attracting chemokines MCP-1, MIP-1 alpha, and IP-10, with corresponding gene expression patterns as determined by Northern blot analysis. In striking contrast, the expression and release of the neutrophil chemoattractant IL-8 was not inducible. To determine the underlying mechanisms responsible for the induction of this differential chemokine pattern, we stimulated monocytes with UV- and heat-inactivated (56 degrees C and 100 degrees C) influenza A virus. In comparison with fully infectious influenza A, 56 degrees C-inactivated virus induced a strong production of MCP-1, MIP-1 alpha, and IP-10, while the release of MIP-1 alpha and IP-10 was substantially lower after exposure to UV-inactivated virus. No chemokine expression was found after stimulation with 100 degrees C-inactivated influenza A virus. Our data indicate that, contingent upon the chemokine examined, the maximal induction depends on the unrestricted infectivity of the virus, the unaltered hemagglutinin molecule, or the intact viral RNA. This diversified chemokine production may enable the infected host to mount an efficient antiviral response against infective and noninfective virus particles.
人单核细胞感染甲型流感病毒后,我们发现单核细胞趋化因子MCP-1、MIP-1α和IP-10迅速且显著释放,通过Northern印迹分析确定了相应的基因表达模式。与之形成鲜明对比的是,中性粒细胞趋化因子IL-8的表达和释放无法被诱导。为了确定导致这种趋化因子差异模式诱导的潜在机制,我们用紫外线和热灭活(56℃和100℃)的甲型流感病毒刺激单核细胞。与完全感染性的甲型流感相比,56℃灭活病毒诱导MCP-1、MIP-1α和IP-10大量产生,而暴露于紫外线灭活病毒后MIP-1α和IP-10的释放则显著降低。用100℃灭活的甲型流感病毒刺激后未发现趋化因子表达。我们的数据表明,根据所检测的趋化因子不同,最大诱导作用取决于病毒的无限制感染性、未改变的血凝素分子或完整的病毒RNA。这种多样化的趋化因子产生可能使受感染宿主能够对感染性和非感染性病毒颗粒发起有效的抗病毒反应。