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1 Respiratory Research Group and Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
2 Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA
* To whom correspondence should be addressed. E-mail: dproud{at}ucalgary.ca.
Human rhinovirus (HRV) infections trigger exacerbations of asthma and chronic obstructive pulmonary disease (COPD), and are associated with lymphocytic infiltration of the airways. We demonstrate that infection of primary cultures of human airway epithelial cells, or of the BEAS-2B human bronchial epithelial cell line, with human rhinovirus type 16 (HRV-16) induces expression of IP-10 (CXCL10), a ligand for the CXCR3 receptor found on activated Type-1 T-lymphocytes and natural killer cells. IP-10 mRNA reached maximal levels 24 h after HRV-16 infection then declined, while protein levels peaked 48 h after infection with no subsequent new synthesis. Cytosolic levels of AU-rich factor 1 (AUF1), a protein associated with mRNA destabilization, increased beginning 24 h after HRV-16 infection. Generation of IP-10 required virus capable of replication, but was not dependent on prior induction of Type 1 interferons. Transfection of synthetic double-stranded RNA into epithelial cells induced robust production of IP-10, while transfection of single-stranded RNA had no effect. Induction of IP-10 gene expression by HRV-16 depended upon activation of NF-
B, as well as other transcription factor recognition sequences further upstream in the IP-10 promoter. In vivo infection of human volunteers with HRV-16 strikingly increased IP-10 protein in nasal lavages during symptomatic colds. Levels of IP-10 correlated with symptom severity, viral titer and numbers of lymphocytes in airway secretions. Thus, IP-10 may play a role in the pathogenesis of HRV-induced colds and in HRV-induced exacerbations of COPD and asthma.
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