title: Reduced spontaneous apoptosis in peripheral blood neutrophils during exacerbation of COPD.
abstract: A major feature of acute exacerbation of chronic obstructive pulmonary disease (COPD) is the accumulation of activated neutrophils in the bronchial tree. This phenomenon can be explained by an increased migration and/or by a prolonged survival due to an inhibition of spontaneous apoptosis. The aim of this study was to assess the apoptotic behaviour of peripheral blood neutrophils in COPD patients during an acute exacerbation. Thirty-six hospitalised COPD patients with an acute exacerbation and 10 healthy volunteers were included. Blood samples were obtained at admission, after 3-5 days and at discharge. Spontaneous apoptosis of isolated neutrophils was measured based on Annexin V-PE binding and nuclear morphology after culturing for 18 h. At admission, significantly lower rates of spontaneous apoptosis were noted in COPD patients compared with healthy volunteers (mean +/- SD 31 +/- 13% versus 44 +/- 18%). The mean percentages of apoptotic neutrophils were 31 +/- 13% at admission, 39 +/- 15% after 3-5 days and 47 +/- 18% at discharge. There was a statistically significant difference between the rates of spontaneous apoptosis on the first day and at discharge. Neither forced expiratory volume in one second < 35% predicted, smoking habit, corticosteroid therapy nor evidence of bacterial infection showed any influence on the spontaneous apoptosis in this study. In conclusion, during acute exacerbations of chronic obstructive pulmonary disease, neutrophil granulocytes show a reduced spontaneous apoptosis that increases progressively after treatment and clinical remission. This raises the question of the importance of neutrophil apoptosis in the development and resolution of exacerbations of chronic obstructive pulmonary disease.
authors.affiliation: Dept of Chest and Infectious Diseases, City Hospital Emil von Behring Affil. Freie Universitaet Berlin, Germany.
authors.forename: M W R
authors.initials: MW
authors.lastname: Pletz
authors.forename: M
authors.initials: M
authors.lastname: Ioanas
authors.forename: A
authors.initials: A
authors.lastname: de Roux
authors.forename: O
authors.initials: O
authors.lastname: Burkhardt
authors.forename: H
authors.initials: H
authors.lastname: Lode
mesh_terms: D000368:Aged; D017209:Apoptosis / Q000502:physiology*; D001980:Bronchi / Q000473:pathology; D002465:Cell Movement / Q000502:physiology; D002467:Cell Nucleus / Q000648:ultrastructure; D002470:Cell Survival / Q000502:physiology; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume / Q000502:physiology; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D008297:Male; D018375:Neutrophil Activation / Q000502:physiology; D009504:Neutrophils / Q000502:physiology*; D011239:Prednisolone / Q000627:therapeutic use; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D012074:Remission Induction; D012907:Smoking / Q000503:physiopathology; D013183:Sputum / Q000382:microbiology
chemical_list: D005938:Glucocorticoids; D011239:Prednisolone