RSV-infected airway epithelial cells cause biphasic up-regulation of CCR1 expression on human monocytes
| Autor: | Lynette H. Thomas, Jon S. Friedland, Paul T. Morrison, Mike Sharland |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
CCR1
Chemokine Cytochalasin D Receptors CCR2 Receptors CCR3 Immunology CCR3 Receptors CCR1 Respiratory Mucosa Cycloheximide Biology Monocytes Proinflammatory cytokine chemistry.chemical_compound Chemokine receptor medicine Humans Immunology and Allergy Cells Cultured Cytoskeleton Tumor Necrosis Factor-alpha Macrophages Monocyte Epithelial Cells Cell Biology Respiratory Syncytial Viruses Up-Regulation Cell biology medicine.anatomical_structure chemistry Culture Media Conditioned Dactinomycin biology.protein Receptors Chemokine Tumor necrosis factor alpha Interleukin-1 |
| Zdroj: | Journal of Leukocyte Biology. 81:1487-1495 |
| ISSN: | 1938-3673 0741-5400 |
| DOI: | 10.1189/jlb.1006611 |
| Popis: | 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 up-regulation 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 CCR1 protein, and CCR1 up-regulation was inhibited by actinomycin D and cycloheximide, indicating that both waves of RSV-CM-induced surface CCR1 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-α (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 inhibition=32±7.2% at 36 h and 23±2.9% at 96 h). In summary, RSV-CM causes a biphasic up-regulation of surface CCR1 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-α and IL-1. |
| Databáze: | OpenAIRE |
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