Longer telomere length in COPD patients with α1-antitrypsin deficiency independent of lung function

• Published in: PloS one Vol. 9; no. 4; p. e95600
• Main Authors: Saferali, Aabida, Lee, Jee, Sin, Don D, Rouhani, Farshid N, Brantly, Mark L, Sandford, Andrew J
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 24.04.2014; Public Library of Science (PLoS)
• Subjects: Adult; Airway management; alpha 1-Antitrypsin Deficiency - genetics; alpha 1-Antitrypsin Deficiency - physiopathology; Biology and Life Sciences; Blood; Blood cells; Case-Control Studies; Cell cycle; Cell division; Chronic obstructive pulmonary disease; Cytokines; Deoxyribonucleic acid; DNA; Emphysema; Female; Forced Expiratory Volume; Genetic testing; Hospitals; Humans; Lung - pathology; Lung - physiopathology; Lungs; Male; Medicine and Health Sciences; Middle Aged; Organ Specificity; Oxidative stress; Pathogenesis; Patients; Peripheral blood; Physical Sciences; Pulmonary Disease, Chronic Obstructive - genetics; Pulmonary Disease, Chronic Obstructive - physiopathology; Respiratory function; Respiratory tract; Senescence; Studies; Telomerase; Telomere - genetics; Telomere Homeostasis; Canada; Florida; Vancouver British Columbia Canada; United States > US
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0095600

Oxidative stress is involved in the pathogenesis of airway obstruction in α1-antitrypsin deficient patients. This may result in a shortening of telomere length, resulting in cellular senescence. To test whether telomere length differs in α1-antitrypsin deficient patients compared with controls, we measured telomere length in DNA from peripheral blood cells of 217 α1-antitrypsin deficient patients and 217 control COPD patients. We also tested for differences in telomere length between DNA from blood and DNA from lung tissue in a subset of 51 controls. We found that telomere length in the blood was significantly longer in α1-antitrypsin deficient COPD patients compared with control COPD patients (p = 1×10(-29)). Telomere length was not related to lung function in α1-antitrypsin deficient patients (p = 0.3122) or in COPD controls (p = 0.1430). Although mean telomere length was significantly shorter in the blood when compared with the lungs (p = 0.0078), telomere length was correlated between the two tissue types (p = 0.0122). Our results indicate that telomere length is better preserved in α1-antitrypsin deficient COPD patients than in non-deficient patients. In addition, measurement of telomere length in the blood may be a suitable surrogate for measurement in the lung.