Molecular characterization of redox mechanisms in allergic asthma

To investigate the molecular redox mechanisms in allergic asthma and to examine current studies of the disease to provide a basis for further investigation of oxidative stress in allergic asthma and the signaling cascades involved in its pathogenesis.

Through the use of PubMed, a broad biomedical literature review was conducted in the following areas related to the physiology and pathobiology of asthma: redox therapy, reactive oxygen species (ROS), oxidative stress, allergic asthma, and antioxidants.

Studies pertaining to oxidative stress and redox signaling in the molecular pathways of inflammation and hypersensitivity in the pathogenesis of allergic asthma were reviewed.

Allergic asthma is associated with an increase in endogenous ROS formation, leading to oxidative stress-induced damage to the respiratory system and mitigated antioxidant defenses. Exposure to environmental antigens has been shown to stimulate overproduction of ROS, resulting in abnormal physiologic function of DNA, proteins, and lipids that clinically can augment bronchial hyperresponsiveness and inflammation. Through the use of animal and human studies, oxidative stress has been determined to be important in the pathogenesis of allergic asthma. Thus, recent research suggests that the assessment of oxidative stress byproducts represents a novel method by which disease severity can be monitored. In addition, the use of redox-based therapy to attenuate levels of ROS presents a potential strategy to alleviate oxidative stress-induced airway inflammation in patients with asthma.

Redox mechanisms of oxidative stress in allergic asthma appear to play a key role in the pathogenesis of the disease and represent a promising therapeutic target.