Avail Biomedical Research Institute

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Asthma is a common inflammatory disorder of the airways, affecting about 300 million people worldwide.

Asthmatic individuals are frequently allergic and show an exaggerated response to environmental agents that are either innocuous or cause only transient inflammatory reactions in the airways of normal subjects. The primary pathogenetic alterations that predispose to this hyperresponsiveness are still largely unknown. Possible candidates are intrinsic defects of the airway epithelium, which would favor the frequently observed sensitization to a number of airborne antigens and the development of inflammatory reactions by allowing the penetration of antigens and irritants through the dysfuntional epithelial barrier.

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The bronchial mucosa of asthmatic patients shows structural and functional alterations of the epithelium, inflammation, accumulation of myofibroblasts below the epithelial basement membrane, and excessive deposition of extracellular matrix molecules in the lamina reticularis. It resembles a wounded tissue where neither the inflammatory phase nor the reparative phase resolve completely.

The current approach to asthma treatment is unsatisfactory because it is directed to suppressing the clinical manifestations of inflammation and airway remodeling rather than preventing or reversing primary pathogenetic alterations.  

 

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