What is obliterative airway disease (OAD)?

Obliterative airway disease (OAD), also known as bronchiolitis obliterans, is a condition that affects the small airways in the lungs, called bronchioles. In this disease, the bronchioles become inflamed and scarred, leading to narrowing or obstruction of the airways. This narrowing can make it difficult for air to flow freely in and out of the lungs, leading to symptoms such as shortness of breath, coughing, and wheezing.


Obliterative airway disease can be caused by various factors, including:


  • Infections: Severe respiratory infections, particularly those caused by certain viruses or bacteria, can lead to inflammation and scarring of the bronchioles.


  • Inhalation of Harmful Substances: Exposure to certain chemicals, toxins, or pollutants, such as those found in cigarette smoke, industrial fumes, or environmental pollutants, can damage the airways and contribute to the development of obliterative airway disease.


  • Lung Transplantation: Obliterative airway disease can also occur as a complication of lung transplantation, where the body’s immune system attacks the transplanted lung tissue, leading to inflammation and scarring of the airways.


  • Autoimmune Diseases: Certain autoimmune diseases, such as rheumatoid arthritis or systemic lupus erythematosus, can cause inflammation in the airways, leading to obliterative airway disease.


What is the relationship between OAD and oxidative stress?

Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them or repair the resulting damage. In the context of OAD, oxidative stress can play a significant role in the development and progression of the disease through various mechanisms:


  • Inflammation: Chronic inflammation is a hallmark of OAD, contributing to the destruction and scarring of the small airways (bronchioles). Inflammatory processes generate ROS as part of the immune response, leading to oxidative stress and tissue damage. ROS can further exacerbate inflammation, creating a vicious cycle that contributes to the progression of OAD.


  • Environmental Exposures: Exposure to environmental pollutants, cigarette smoke, or occupational hazards can increase oxidative stress in the lungs, promoting the development of OAD. These exposures can lead to the generation of ROS, which can damage the airway epithelium and trigger inflammatory responses, ultimately leading to airway remodeling and fibrosis characteristic of OAD.


  • Ischemia-Reperfusion Injury: In the context of lung transplantation, ischemia-reperfusion injury occurs when the transplanted lung is deprived of oxygen during the transplantation process and then reperfused with oxygenated blood upon transplantation. This process can lead to the generation of ROS, oxidative stress, and subsequent damage to the lung tissue, contributing to the development of OAD in transplant recipients.


  • Antioxidant Defenses: Antioxidants are molecules that help neutralize ROS and protect cells from oxidative damage. In OAD, the antioxidant defenses may be overwhelmed or compromised, leading to increased oxidative stress and tissue injury. Decreased levels of antioxidants or impaired antioxidant enzyme activity have been observed in patients with OAD, further exacerbating oxidative stress and contributing to disease progression.