title: Increased serum TRAIL and DR5 levels correlated with lung function and inflammation in stable COPD patients.
abstract: BACKGROUND
  Chronic obstructive pulmonary disease (COPD) is associated with abnormal systemic inflammation, and apoptosis is one of the pathogenic mechanisms of COPD. Several studies have suggested that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its receptors were not only involved in diseases associated with apoptosis but also in inflammatory diseases. However, limited data about the possible relationship between COPD and TRAIL/TRAIL-receptors are available.
  
  
  OBJECTIVE
  To evaluate the potential relationship between TRAIL/TRAIL-receptors and COPD.
  
  
  METHODS
  Serum levels of TRAIL, decoy receptor 5 (DR5), C-reactive protein, and tumor necrosis factor-α were analyzed using multiplex enzyme-linked immunosorbent assay kits. Then, serum levels of TRAIL and DR5 in 57 COPD patients with 35 healthy controls were compared and correlated with lung function and systemic inflammation.
  
  
  RESULTS
  Mean levels of serum TRAIL and DR5 were significantly higher in COPD patients than those in controls (50.17±17.70 versus 42.09±15.49 pg/mL, P=0.029; 48.15±22.88 versus 38.94±10.95 pg/mL, P=0.032, respectively). Serum levels of TRAIL and DR5 correlated inversely with forced expiratory volume in 1 second % predicted, an index of lung function in COPD (r=-0.354, P=0.007 for TRAIL; r=-0.394, P=0.002 for DR5) in all participants (r=-0.291, P=0.005 for TRAIL; r=-0.315, P=0.002 for DR5), while DR5 correlated positively with C-reactive protein (r=0.240, P=0.021 for total subjects) and TRAIL correlated positively with tumor necrosis factor-α (r=0.371, P=0.005 for COPD; r=0.349, P=0.001 for total subjects).
  
  
  CONCLUSIONS
  Our results suggested that circulating TRAIL and DR5 increased in COPD patients and were associated with lung function and systemic inflammation in COPD. Future studies are needed to verify whether and how TRAIL and its receptors play roles in COPD.
authors.affiliation: Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China ; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu, Sichuan, People's Republic of China.
authors.forename: Yanqiu
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China ; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu, Sichuan, People's Republic of China.
authors.forename: Yongchun
authors.initials: Y
authors.lastname: Shen
authors.affiliation: Department of Laboratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
authors.forename: Junlong
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China ; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu, Sichuan, People's Republic of China.
authors.forename: Chun
authors.initials: C
authors.lastname: Wan
authors.affiliation: Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China ; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu, Sichuan, People's Republic of China.
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.affiliation: Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China ; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu, Sichuan, People's Republic of China.
authors.forename: Dan
authors.initials: D
authors.lastname: Xu
authors.affiliation: Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China ; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu, Sichuan, People's Republic of China.
authors.forename: Ting
authors.initials: T
authors.lastname: Yang
authors.affiliation: Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China ; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Chengdu, Sichuan, People's Republic of China.
authors.forename: Fuqiang
authors.initials: F
authors.lastname: Wen
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000175:diagnosis / Q000276:immunology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood*; D008168:Lung / Q000276:immunology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000175:diagnosis / Q000276:immunology / Q000503:physiopathology; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand / Q000097:blood*; D013147:Spirometry; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000097:blood*; D014797:Vital Capacity
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; D053221:TNF-Related Apoptosis-Inducing Ligand; C505639:TNFRSF10B protein, human; C505653:TNFSF10 protein, human
keywords: apoptosis; chronic obstructive pulmonary disease; decoy receptor 5; inflammation; tumor necrosis factor-related apoptosis-inducing ligand