RSV-infected airway epithelial cells cause biphasic upregulation of CCR1 expression on human monocytes

被引:10
作者
Morrison, Paul T.
Thomas, Lynette H.
Sharland, Mike
Friedland, Jon S.
机构
[1] Hammersmith Hosp, Imperial Coll, Dept Infect Dis & Immunity, London W12 0NN, England
[2] St George Hosp, Sch Med, Pediat Infect Dis Unit, London, England
关键词
cell networks; chemokine; respiratory epithelium; cytokines; transcription; cyloskeleton;
D O I
10.1189/jlb.1006611
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Respiratory syncytial virus (RSV) infection can cause extensive airway inflammation, which is orchestrated by chemokines and their receptors. RSV-infected epithelial cells secrete many cytokines and chemokines, but little is known about regulation of chemokine receptors on target cells. We investigated the effects of conditioned media (CM) from RSV-infected epithelial cells on monocyte CCR1, CCR2, and CCR5 expression. RSV-CM but not control-CM stimulated a biphasic increase in cell-surface CCR1, and levels peaked at 36 h and 96 h poststimulation. Similar CCR1 upregulation occurred on monocyte-derived macrophages. Cytochlasin D and colchicine blocked both peaks of expression, demonstrating requirement of a functional cytoskeleton. Intracellular staining revealed little internal sequestration of CCRI protein, and CCRI up-regulation was inhibited by actinomycin D and cycloheximide, indicating that both waves of RSV-CM-induced surface CCRI expression were dependent on de novo transcription and protein synthesis. Cytokine-neutralizing experiments showed that the effects of RSV-CM were decreased by blocking TNF-alpha (percent inhibition=51 +/- 2.3% at 36 h peak and 42 +/- 7.7% at 96 h peak) and to a lesser extent, IL-1 (percent inbibition=32 +/- 7.2% at 36 h and 23 +/- 2.9% at 96 h). In summary, RSV-CM causes a biphasic up-regulation of surface CCRI on monocytes, which is dependent on an intact cytoskeleton, requires new gene transcription and protein synthesis, and is mediated in part by the proinflammatory cytokines TNF-alpha and IL-1.
引用
收藏
页码:1487 / 1495
页数:9
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