Mumps virus inhibits migration of primary human macrophages toward a chemokine gradient through a TNF-alpha dependent mechanism.
Mumps virus inhibits migration of primary human macrophages toward a chemokine gradient through a TNF-alpha dependent mechanism.
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腮腺炎病毒通过 TNF-α 依赖性机制抑制原代人类巨噬细胞向趋化因子梯度迁移。
DOI：
10.1016/j.virol.2012.08.017
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Parks,GriffithD
中科院分区：
文献类型：
--
作者：
Briggs,CaitlinM;Mayer,AnneE;Parks,GriffithD
巨噬细胞是一种重要的免疫调节细胞，在病毒的致病机制中发挥重要作用。在这里，我们解决的影响，原代人类巨噬细胞感染相关的副粘病毒副流感病毒5（PIV 5）和腮腺炎病毒（MuV）。用PIV 5或MuV感染的单核细胞衍生的巨噬细胞表现出非常小的细胞病变效应，但发现在向趋化因子如巨噬细胞集落刺激因子（MCSF）和血管内皮生长因子（VEGF）的梯度迁移方面存在缺陷。对于MuV感染，迁移的抑制需要活病毒感染，但不是由感染细胞表面上的趋化因子受体的损失引起的。MuV介导的巨噬细胞趋化性的抑制是通过从感染的细胞释放的可溶性因子。MuV感染可增加TNF-α的分泌，但对巨噬细胞抑制因子（MIF）无明显影响。抗体抑制和反向添加实验表明，TNF-α是MuV介导的趋化抑制的必要和充分条件。
Macrophages are an important cell type for regulation of immunity, and can play key roles in virus pathogenesis. Here we address the effect of infection of primary human macrophages with the related paramyxoviruses Parainfluenza virus 5 (PIV5) and Mumps virus (MuV). Monocyte-derived macrophages infected with PIV5 or MuV showed very little cytopathic effect, but were found to be defective in migration toward a gradient of chemokines such as macrophage colony stimulating factor (MCSF) and vascular endothelial growth factor (VEGF). For MuV infection, the inhibition of migration required live virus infection, but was not caused by a loss of chemokine receptors on the surface of infected cells. MuV-mediated inhibition of macrophage chemotaxis was through a soluble factor released from infected cells. MuV infection enhanced secretion of TNF-α, but not macrophage inhibitory factor (MIF). Antibody inhibition and add-back experiments demonstrated that TNF-α was both necessary and sufficient for MuV-mediate chemotaxis inhibition.