Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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Published online before print March 27, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1006611

Received for publication October 6, 2006.
Revised February 7, 2007.
Accepted for publication February 12, 2007.

Article

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

Paul T. Morrison *, Lynette H. Thomas *, Mike Sharland {dagger}, and Jon S. Friedland *@

*Department of Infectious Diseases & Immunity, Imperial College, Hammersmith Campus, London, United Kingdom; and {dagger}Pediatric Infectious Diseases Unit, St George’s Hospital Medical School, London, United Kingdom

@ To whom correspondence should be addressed. E-mail: j.friedland{at}imperial.ac.uk.


  Abstract

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-{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 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-{alpha} and IL-1.

Key Words: cell networks • chemokine • respiratory epithelium • cytokines • transcription • cytoskeleton




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