Abstract
Background Many aeroallergens activate PAR-2 receptors on the airway epithelium. We have shown that PAR-2 activation participates in allergic sensitization and allergic airway inflammation in animal models of asthma. Moreover, PAR-2 is upregulated on the airway epithelium of asthmatics, but the mechanisms and factors responsible are unknown. As asthmatic airways are under various types of physiological stress, we hypothesized that cellular stress upregulates PAR-2 on airway epithelium and this upregulation is functional. Methods
Highlights
Many aeroallergens activate proteinase activated receptor – 2 (PAR-2) receptors on the airway epithelium
As asthmatic airways are under various types of physiological stress, we hypothesized that cellular stress upregulates PAR-2 on airway epithelium and this upregulation is functional
We have previously shown that growth factor deprivation, but not oxidative stress or hypoxia, significantly upregulates PAR-2 mRNA in normal bronchial epithelial cells
Summary
Many aeroallergens activate PAR-2 receptors on the airway epithelium. We have shown that PAR-2 activation participates in allergic sensitization and allergic airway inflammation in animal models of asthma. PAR-2 is upregulated on the airway epithelium of asthmatics, but the mechanisms and factors responsible are unknown. As asthmatic airways are under various types of physiological stress, we hypothesized that cellular stress upregulates PAR-2 on airway epithelium and this upregulation is functional
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