Abstract
Background Young children who experience human rhinovirus (HRV)-associated wheezing illnesses are more likely to develop subsequent asthma [1]. This has led to the hypothesis that HRV infection may be involved in the pathogenesis of airway remodeling in asthma [2]. Increased airway smooth muscle (ASM) mass, in which ASM cells are in close proximity to the subepithelial region, is a characteristic feature of airway remodeling [3]. We have shown that HRV infection of human bronchial epithelial (HBE) cells, both in vitro and in vivo, results in the upregulation of airway remodeling mediators [4]. We now sought to determine whether HRV infection of HBE cells is associated with airway smooth muscle (ASM) chemotaxis.
Highlights
Young children who experience human rhinovirus (HRV)-associated wheezing illnesses are more likely to develop subsequent asthma [1]
Primary human bronchial epithelial (HBE) cells pre-treated with medium containing 1% insulin, transferrin, and selenium (ITS) for 24 hours were exposed to medium or purified HRV-16 (MOI: 0.3-1) for 24 hours
HBE cell supernatants were studied as chemoattractants for airway smooth muscle (ASM) chemotaxis
Summary
Young children who experience human rhinovirus (HRV)-associated wheezing illnesses are more likely to develop subsequent asthma [1]. This has led to the hypothesis that HRV infection may be involved in the pathogenesis of airway remodeling in asthma [2]. Increased airway smooth muscle (ASM) mass, in which ASM cells are in close proximity to the subepithelial region, is a characteristic feature of airway remodeling [3]. We have shown that HRV infection of human bronchial epithelial (HBE) cells, both in vitro and in vivo, results in the upregulation of airway remodeling mediators [4]. We sought to determine whether HRV infection of HBE cells is associated with airway smooth muscle (ASM) chemotaxis
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