Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/17338
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Type: Journal article
Title: Increased airway epithelial and T-cell apoptosis in COPD remains despite smoking cessation
Author: Hodge, S.
Hodge, G.
Holmes, M.
Reynolds, P.
Citation: European Respiratory Journal, 2005; 25(3):447-454
Publisher: European Respiratory Soc Journals Ltd
Issue Date: 2005
ISSN: 0903-1936
1399-3003
Abstract: There is heterogeneity in the propensity of smokers to develop chronic obstructive pulmonary disease (COPD), and improved treatment strategies are hindered by limited understanding of COPD pathogenesis, especially as distinct from the effects of smoking per se. Although apoptosis is essential for tissue homeostasis, increased apoptosis may cause tissue damage and inflammation. This study addressed whether airway T-lymphocytes and airway epithelial cells (AEC) show an increased likelihood of undergoing apoptosis in COPD and if this was related to smoking. Apoptosis (7-amino-actinomycin D, Annexin, single-stranded DNA and caspase), Bcl-2, Bax and p53 were assessed in cells obtained from bronchial bushing and bronchoalveolar lavage from ex- and continuing smokers with COPD, and nonsmoking controls, using flow cytometry. A mean 87% increase in apoptosis of AEC and a 103% increase in T-lymphocyte apoptosis were found in COPD. There were no significant differences in apoptosis of AEC between current and ex-smokers with COPD. Apoptosis may contribute to chronic obstructive pulmonary disease pathogenesis, and continued excess apoptosis after smoking cessation may offer a new target for therapeutic interventions. Whether the persistence of increased apoptosis after smoking cessation results from changes in the pulmonary milleau after years of noxious insult, or whether some individuals have a natural predisposition toward increased apoptosis and possible development of chronic obstructive pulmonary disease remains to be determined.
Keywords: Respiratory Mucosa
Leukocytes
T-Lymphocytes
Bronchoalveolar Lavage Fluid
Humans
Pulmonary Disease, Chronic Obstructive
Necrosis
L-Lactate Dehydrogenase
Proto-Oncogene Proteins c-bcl-2
Smoking
Smoking Cessation
Age Factors
Apoptosis
Aged
Middle Aged
Tumor Suppressor Protein p53
bcl-2-Associated X Protein
DOI: 10.1183/09031936.05.00077604
Appears in Collections:Aurora harvest 6
Paediatrics publications

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