Chronic Obstructive Pulmonary Disease (COPD) is a major, global health problem and has only begun to be studied to a significant extent within the past two decades. Projections indicate that COPD may become the third most common cause of death and fifth most common cause of disability worldwide by 2020 (Burney et al, 2014). COPD is characterized by irreversible damage, obstruction, and infiltration of bronchioles and lung parenchyma, causing airflow limitation in patients.
The immune system is responsible for fighting infection and cleaning up the body in response to physiological stresses. “Inflammation” refers to the immune system’s response to these harmful stimuli (infection, pathogens, damage, irritants). Some cells involved in the inflammatory process include neutrophils, macrophages, T-cells, and eosinophils, among others. In summary, in response to an infection or in the presence of irritants, these cells can release factors that can fight off the pathogens and neutralize the irritants in order to protect the body.
Neutrophils, as an example, release several proteases during the inflammatory response. While these can help fight against things like bacterial infection, they can act on many kinds of proteins in close proximity. In the case of COPD, some of these proteases can break down proteins located in lung parenchyma and/or bronchioles, causing damage to the lungs. In addition, some inflammatory cells can release reactive oxygen species (ROS) as a defense mechanism. These ROS can also damage lung tissue (in addition to their normal and beneficial inflammatory effects).
Cigarette smoking is currently the most significant risk factor (by far) for COPD. Cigarette smoke creates many irritants that, when inhaled, can trigger inflammation in the lungs, recruiting the cells noted previously (neutrophils, macrophages, T-cells, eosinophils), which can secondarily cause irreversible lung damage, resulting in COPD. The same effects can occur with exposure to air pollution and even viral infections such as adenovirus (Morimoto et al, 2009). The presence of these irritants also recruits more inflammatory cells, which themselves can obstruct bronchioles.
Luckily, we have a way of protecting our lung tissue from possible damage from ROS and proteases, in the form of anti-oxidants and anti-proteases, such as α1‐antitrypsin. However, this also means that individuals with α1‐antitrypsin deficiency are at an increased risk for COPD. In contrast to external risk factors (cigarette smoking, pollution, respiratory infection), α1‐antitrypsin deficiency is currently the only known host risk factor (Barnes et al, 2003).
Currently, there is no known and proven treatment for COPD. The lung tissue damage by these proteases and ROS is irreversible, and the narrowing of airways is also untreatable at this time. Unlike asthma, steroids do not offer relief of symptoms in COPD.