Abstract
Background The prevalence of allergic asthma has increased dramatically over the last 20 years. Environmental allergens such as house dust mites (HDM), cockroach, fungi and pollens are major asthma triggers. Recent studies indicate that the serine proteinase activity of these allergens is an important factor contributing to their ability to induce airway inflammation. Allergen serine proteinases can activate Proteinase Activated Receptor -2 (PAR-2), a G protein coupled receptor, which is upregulated on the airway epithelium of asthmatics. PAR-2 activation is pro-inflammatory in many biological systems. PAR-2 polymorphisms are associated with the development of atopy. We have shown that allergic sensitization and inflammation in mouse models of asthma is PAR-2 dependent. We have proposed that PAR-2 on the airway epithelium is a sensor for environmental allergens and leads to allergic inflammation. However, the regulation of PAR-2 expression on airway epithelium is poorly studied. As asthmatic airways are under various types of cellular stress, we hypothesized that cellular stress regulates PAR-2 on airway epithelium. Methods
Highlights
The prevalence of allergic asthma has increased dramatically over the last 20 years
Allergen serine proteinases can activate Proteinase Activated Receptor -2 (PAR-2), a G protein coupled receptor, which is upregulated on the airway epithelium of asthmatics
We have proposed that PAR-2 on the airway epithelium is a sensor for environmental allergens and leads to allergic inflammation
Summary
The prevalence of allergic asthma has increased dramatically over the last 20 years. Environmental allergens such as house dust mites (HDM), cockroach, fungi and pollens are major asthma triggers. Allergen serine proteinases can activate Proteinase Activated Receptor -2 (PAR-2), a G protein coupled receptor, which is upregulated on the airway epithelium of asthmatics. We have shown that allergic sensitization and inflammation in mouse models of asthma is PAR-2 dependent. We have proposed that PAR-2 on the airway epithelium is a sensor for environmental allergens and leads to allergic inflammation. The regulation of PAR-2 expression on airway epithelium is poorly studied. As asthmatic airways are under various types of cellular stress, we hypothesized that cellular stress regulates PAR-2 on airway epithelium
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