Chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema, is characterized by chronic and progressive airflow limitation. It affects more than 16 million Americans, is the fourth leading cause of death in the United States.
COPD is caused by abnormal inflammatory response of the lungs to cigarette smoking, air pollution, working for many years in a dusty environment, and frequent bacterial infections of the upper respiratory system. When the lungs are irritated by noxious particles or gases, they swell and produce a large amount of mucus. If inflammation persists for a long period, the protease enzymes released by inflammatory cells can damage the walls of the airways and cause airway obstruction.
COPD Involves Systemic Inflammation
A large number of studies suggest that COPD involves not only inflammatory response in the airway and the lungs, but also systemic inflammation. It has been established that stable COPD is associated with low-level systemic inflammation as demonstrated by an increase in CRP (inflammatory marker) and cytokines (small proteins that affect communications, growth and death of cells). The levels of inflammatory markers are inversely related to airflow limitation.
During acute exacerbations of COPD (worsening of COPD symptoms), the inflammatory response is further increased. Systemic inflammation induces oxidative stress, damages cellular proteins, membrane and DNA, and results in widespread effects.
Systemic Inflammation Increases Cardiovascular Injury in COPD
It is well established that cigarette smoke increases the risk of cardiovascular disease (CVD). Smokers with COPD have a higher risk of CVD comparing those with no COPD. This risk increases with increased severity of COPD and is highest among people hospitalized for COPD.
In patients with established cardiovascular disease, COPD is associated with increased cardiovascular events, i.e., heart attack, irregular heartbeat, and heart failure. Emerging evidence suggests that increased oxidative stress that occurs during exacerbations of COPD, together with the enhanced systemic inflammatory response, have direct harmful effects on cardiac muscles and arteries. It has been well established that increased inflammatory response destabilizes atherosclerotic plaques, promotes clot formation and triggers heart attack.
Systemic Inflammation Leads to Skeletal Muscle Dysfunction in COPD
COPD is a disease that is not confined to the airways and the lungs. It is considered a complex, systemic disease involving several organs and systems. Skeletal muscle dysfunction in COPD is apparent which is characterized by a reduction in muscle strength and loss of muscle mass. Loss of muscle mass is a complex process that involves changes in protein metabolism and muscle cell turnover. Impaired protein metabolism may result in muscle atrophy when protein degradation exceeds protein synthesis.
Abundant evidence indicates that increased inflammatory response contributes to muscle atrophy by increasing protein degradation and cell death, and reducing protein synthesis and cell regeneration. Other factors include poor nutrition, inactivity, heart failure, and reduced antioxidant defenses.
Control of Inflammation Offers a Whole Body Approach To COPD
There is no cure for COPD. Current treatments focus on relieving symptoms: bronchodilators relaxe the bronchial muscles so the airways are widened for easier to breathe; antibiotics reduce bacterial infection, and steroids help relax the airways and make breathe easier. These drugs usually are not prescribed for long-term use because of their side effects. Furthermore, they do not influence inflammatory response and have no positive impact on other organ dysfunctions.