Study Suggests a Link Between Mitochondrial Dysfunction in Leukocytes and Chronic Obstructive Pulmonary Disease (COPD)
A new study published in the journal PLOS One suggests a link between mitochondrial dysfunction in important immune cells called leukocytes and the development of chronic obstructive pulmonary disease (COPD). The study is entitled “Leukocyte Mitochondrial DNA Copy Number Is Associated with Chronic Obstructive Pulmonary Disease” and was led by researchers at Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine in Taiwan.
COPD is one of the most common lung diseases and a major cause of morbidity and mortality worldwide, being the third leading cause of death in the United States. It is a progressive disease in which individuals develop serious problems in breathing with obstruction of the airways, shortness of breath (dyspnea), cough and acute exacerbations. Smoking is considered to be the leading cause of COPD and the disease can seriously impact the patient’s physical capacity, well-being and social functioning.
COPD pathogenesis is known to be linked to oxidative stress, an imbalance between the generation of free radicals and reactive oxygen and nitrogen species (ROS and RNS), which can damage important cellular components, and the body’s ability to counteract their harmful effects by antioxidant mechanisms.
Mitochondria, cellular organelles where the energy for the body is produced, are highly susceptible to ROS. Mitochondria have their own DNA, but they have limited DNA repair capacity and compensate for the damage by increasing the number of mtDNA copies. It has been shown that mitochondrial changes and dysfunction in patients with COPD may potentially be the result of long-term exposure to cigarette smoke.
In the study, researchers hypothesized that the copy number of mitochondrial DNA in peripheral leukocytes (white blood cells important for immunity) may be a response to ROS and represent a biomarker for the development of COPD. The team analyzed the mitochondrial DNA copy number from peripheral leukocytes of 86 COPD patients, 77 non-smokers and 33 healthy smokers.
Researchers found that the mitochondrial DNA copy number in leukocytes was significantly inferior in COPD patients compared to non-smokers and healthy smokers, who had a similar copy number. In addition, the serum glutathione level (an antioxidant) in COPD patients was also found to be lower in comparison to healthy smokers and non-smokers, suggesting a reduced antioxidant capacity in COPD patients that may lead to leukocytes mitochondrial dysfunction.
Based on their findings, the research team concluded that COPD is linked to a decrease in leukocyte mitochondrial DNA copy number, as well as serum glutathione levels. The authors suggest that mitochondrial dysfunction and ROS from cigarette smoke may promote inflammation and the onset of COPD, and that therapies based on antioxidant strategies might be valuable for the management of mitochondrial dysfunction associated with COPD. The team, however, states that further studies are required to understand the mechanism linking COPD to mitochondrial dysfunction.