Published ahead of print on February 14, 2008, doi:10.1164/rccm.200708-1243OC Am. J. Respir. Crit. Care Med., Volume 177, Number 10, May 2008, 1111-1121 A more recent version of this article appeared on May 15, 2008
Submitted on August 22, 2007 Human Rhinovirus 1B Exposure Induces PI 3-kinase-dependent Airway Inflammation in MiceDawn C Newcomb1,1 Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA, 2 Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, USA, 3 Department of Pathology, University of Michigan, Ann Arbor, MI, USA, 4 Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London, United Kingdom, 5 Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA; Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, USA * To whom correspondence should be addressed. E-mail: mhershen{at}umich.edu.
Rationale: Infection with rhinovirus (RV) triggers exacerbations of asthma and chronic obstructive lung disease.
Objective: We sought to develop a mouse model of RV employing RV1B, a minor group serotype which binds to the low-density lipoprotein receptor.
Methods: C57BL/6 mice were inoculated intranasally with RV1B, replication-deficient UVirradiated RV1B, or RV39, a major group virus.
Measurements and Main Results: Viral RNA was present in the lungs of RV1B-treated mice, but not those exposed to UV-irradiated RV1B or RV39. Lung homogenates of RV-treated mice contained infectious RV four days after inoculation. RV1B exposure induced neutrophilic and lymphocytic airway inflammation, as well as increased lung expression of KC, macrophageinflammatory protein-2 and interferons- Key words: asthma, COPD, Akt, low-density lipoprotein receptor
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