Abstract
Background Structural cells of the airways are subject to normal mechanical stretch during respiration [1]. Mechanical stretch acts as a mechanism of cell activation, and mechanotransduction pathways have been shown to activate pro-inflammatory genes [2]. Human rhinovirus (HRV) infections are a major cause of asthma exacerbations, and mechanical forces are likely to be more pronounced during asthma exacerbations [3]. Moreover, smoking is associated with worse clinical outcomes in asthma. Previous studies have shown that HRV infection, cigarette smoke extract (CSE), or mechanical stretch each induce CXCL8 production in bronchial epithelial cells [4-6]. In this study, we sought to determine whether mechanical stretch interacts with HRV infection and CSE to further upregulate airway inflammation.
Highlights
Structural cells of the airways are subject to normal mechanical stretch during respiration [1]
Mechanical stretch and Human rhinovirus (HRV) infection each significantly increased CXCL8 release in BEAS-2B and HBE cells compared to static controls (p
Mechanical stretch and HRV infection each increased CXCL8 mRNA levels compared to static controls, with the combination resulting in further enhanced induction (p
Summary
Structural cells of the airways are subject to normal mechanical stretch during respiration [1]. Mechanical stretch acts as a mechanism of cell activation, and mechanotransduction pathways have been shown to activate pro-inflammatory genes [2]. Human rhinovirus (HRV) infections are a major cause of asthma exacerbations, and mechanical forces are likely to be more pronounced during asthma exacerbations [3]. Smoking is associated with worse clinical outcomes in asthma. Previous studies have shown that HRV infection, cigarette smoke extract (CSE), or mechanical stretch each induce CXCL8 production in bronchial epithelial cells [4,5,6]. We sought to determine whether mechanical stretch interacts with HRV infection and CSE to further upregulate airway inflammation
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