Concise Details of RADS | Biomedgrid

Reactive Airways Dysfunction Syndrome (RADS) is an abrupt-onset asthmatic disorder of a non-allergy origin. Its mechanism relies on innate immunity that permits the airways to deal with non-microbiological constituents. The massive exposure causes a severe airway injury with ensuing detachment of damaged and dead epithelial cells. There is the release of Molecules of Damage-Associated Molecular Patterns (DAMPs) by stressed or dying cells. Hematopoietic and bone marrow-derived cells migrate to renew the denuded cellular barrier. Soluble growth factors, interleukins, chemokines, arachidonic acid products, and discharges from airway smooth muscle cells aid epithelial and tissue repair. Metalloproteases and extracellular matrix influence the epithelial-to-mesenchymal matrix. Lung macrophages contribute to the repair and influence airway hyperresponsiveness. Airway wall thickening, subepithelial fibrosis, mucus metaplasia, myofibroblast hyperplasia, muscle cells hyperplasia and hypertrophy, and epithelial hypertrophy are characteristic features of the airway remodeling (136-word count).