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Journal of Virology, May 2006, p. 4521-4527, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4521-4527.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Differential Chemokine Expression following Respiratory Virus Infection Reflects Th1- or Th2-Biased Immunopathology

Fiona J. Culley ,{dagger},{ddagger} Alasdair M. J. Pennycook,{dagger} John S. Tregoning, Tracy Hussell,§ and Peter J. M. Openshaw*

Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, St Mary's Campus, London W2 1PG, United Kingdom

Received 5 December 2005/ Accepted 3 February 2006

Respiratory syncytial virus (RSV) is a major viral pathogen of infants that also reinfects adults. During RSV infection, inflammatory host cell recruitment to the lung plays a central role in determining disease outcome. Chemokines mediate cell recruitment to sites of inflammation and are influenced by, and influence, the production of cytokines. We therefore compared chemokine production in a mouse model of immunopathogenic RSV infection in which either Th1 or Th2 immunopathology is induced by prior sensitization to individual RSV proteins. Chemokine expression profiles were profoundly affected by the nature of the pulmonary immunopathology: "Th2" immunopathology in BALB/c mice was associated with increased and prolonged expression of CCL2 (MCP-1), CXCL10 (IP-10), and CCL11 (eotaxin) starting within 24 h of challenge. C57BL/6 mice with "Th2" pathology (enabled by a deficiency of CD8+ cells) also showed increased CCL2 production. No differences in chemokine receptor expression were detected. Chemokine blockers may therefore be of use for children with bronchiolitis.

* Corresponding author. Mailing address: Department of Respiratory Medicine, Imperial College London, St Mary's Campus, London W2 1PG, United Kingdom. Phone: 44 20 7594 3854. Fax: 44 20 7262 8913. E-mail: p.openshaw{at}imperial.ac.uk.

{dagger} F.J.C. and A.M.J.P. contributed equally to this work.

{ddagger} Present address: Department of Biological Sciences, Imperial College London, South Kensington Campus, London SW7 2AZ, United Kingdom.

§ Present address: The Kennedy Institute, Aspenlea Road, London W6 8LH, United Kingdom.

Journal of Virology, May 2006, p. 4521-4527, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4521-4527.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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