Oxidative stress plays a critical role in maintaining cellular homeostasis and host defense through the oxidation and reduction of molecules. Reactive oxygen species (ROS) such as superoxide and hydrogen peroxide are generated by mitochondria and immune cells in response to pathogens. However, excessive production of oxidants due to inflammation or chronic insults can result in oxidative stress and cell/tissue damage. Oxidative stress has been implicated in many diseases across several systems, including respiratory diseases such as asthma.
Asthma is a chronic obstructive lung disease affecting millions of Americans, characterized by airway inflammation and hyperresponsiveness. Obesity, which is marked by adiposity defined by a body mass index greater than 30 kg/m2, is a significant risk factor for asthma and also causes oxidative stress through inflammation of adipose tissue. Oxidative stress, therefore, could be a major factor in understanding how asthma is altered in the context of obesity.
The airway epithelium, as the primary protective barrier defending the lung, plays a crucial role in maintaining barrier integrity. However, oxidative stress caused by asthma and other lung diseases can cause damage and permeability of the epithelium. Immune cells are recruited to the submucosal area in response to provocative agents, which produce ROS, exacerbating the airway epithelium damage. In patients with obesity and asthma, inflamed adipose tissue contributes to additional oxidative stress, accelerating epithelial damage and barrier permeability.
Understanding the relationship between oxidative stress, obesity, and asthma is crucial for developing effective treatment options that can improve asthma control as obesity rates continue to rise.
