Eighteen Questions for the Better Understanding of RADS

Abstract

RADS are typically associated with a solitary inhalation exposure to a very high concentration of an irritant gas, vapor, aerosol or fume. Evolution of asthma-like symptoms and airway hyperresponsiveness are consequences Prompt medical assistance is needed within the first 24 hours. The manuscript unveils suggested sequences of RADS’ pathogenesis. The airway injury causes sloughing off of damaged and dead airway cells. Putatively, escaping intracellular molecules, from dead and damaged cells, enter the extracellular space as damage-associated molecular patterns (DAMPs); they are also known as “alarmins.” The molecules promote an inflammatory response and orchestrate cellular repair and tissue healing. Different mediators and regulatory intermediaries, chemokines and cytokines, arachidonic acid products, soluble growth factors, prostaglandins, and matrix components take part in regenerative process. Lung macrophages provide clean-up and repair services: and, they impact airway hyperresponsiveness. Metalloproteinases and extracellular matrix improve the epithelial-tomesenchymal matrix. Airway wall thickening, subepithelial fibrosis, mucus metaplasia, myofibroblast hyperplasia, muscle cells hyperplasia and hypertrophy, and epithelial hypertrophy become features of the airway remodeling response.