Reactive oxygen species and obstructive lung disease

Abstract

The respiratory system is constantly exposed to both endogenous and exogenous oxidants. Oxidative stress plays a critical role in the development, progression, monitoring, and, perhaps in the future, the treatment of both asthma and chronic obstructive pulmonary disease. It is estimated that asthma currently affects 300 million people globally, with its prevalence increasing by 50 % every decade. COPD is projected to become the third leading cause of death by 2020. The fundamental pathology in asthma is the interplay between the defective epithelial barrier, the inappropriate immune response to common allergens with the development of chronic inflammation, leading to airway remodeling and asthmatic symptoms. Reactive Oxygen species (ROS) induce airway epithelial dysfunction, resulting in oxidative damage of the underlying tissue, and can skew the immune system to a TH2 type response. The development of COPD has been strongly linked to the chronic inhalation of noxious gases, inducing inflammatory responses and oxidative damage to the lung parenchyma. Oxidative stress alters gene transcription, induces mucous gland hyper-secretion/hyperplasia, and accelerates cellular apoptosis; all these relate closely to the clinical manifestations of COPD. A lack of ability to both detect ROS and develop agents that cure or reverse these diseases means that the global burden of both conditions continues to be a major health issue. However, recent studies demonstrate the potential of exhaled breath condensate in the diagnosis and monitoring of respiratory diseases and may provide a method of measuring airway oxidative stress. Future breakthroughs in antioxidant therapy may provide an alternative pathway in the treatment of both asthma and COPD.