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Tacon C et al. – Electrophoretic mobility shift assays and supershift assays confirmed nuclear translocation and binding of p50/p65 NF–kB subunits to a MMP–9 specific NF–kB oligonucleotide. This increase in MMP–9 may be a mechanism by which rhinovirus infections contribute to airway inflammation and, potentially, to airway remodeling.


Exclusive Author Commentary
Richard Leigh, 10/01/09

Human rhinovirus (HRV) infections are major risk factors for the development of asthma in young children and exacerbations in individuals with established asthma; however the mechanisms by which this occurs are currently unknown. This has led us to hypothesize that HRV infection of human bronchial epithelial (HBE) cells play a role in the development and continued progression of airway inflammation and possibly remodeling. We show that HRV infection, both in vivo and in vitro, disrupts the MMP-9:TIMP-1 ratio by increasing MMP-9 but not TIMP-1 expression. Using pharmacological inhibitors, promoter luciferase constructs, electrophoretic mobility shift assays and supershift assays, we also show that the transcription factor NF-?B is necessary for the increased expression of MMP-9 upon HRV infection. This study provides a possible mechanism by which human rhinovirus (HRV) infections may contribute to the development and continued progression of airway inflammation and remodeling.

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