Pulmonary epithelium, cigarette smoke, and chronic obstructive pulmonary disease.
Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease involving a wide variety of cells and inflammatory mediators. The most important etiological factor in the development of this disease is cigarette smoking. Much of the research into the mechanisms of COPD has been concerned with the induction of inflammation and the role of neutrophils and macrophages in the pathophysiology of the disease. The possible contribution of the epithelium to the development of COPD has only recently become apparent and remains unclear. In this article we review research into the effect of cigarette smoke on the pulmonary epithelium with particular emphasis on oxidative stress, proteolytic load, pro-inflammatory cytokine and chemokine profile and epithelial secretions. In addition, we have also reviewed how cigarette smoke may affect epithelial damage and repair processes.
Thorley
Andrew J
AJ
Lung Cell Biology, Section of Airways Disease, National Heart and Lung Institute, Imperial College, Dovehouse Street, London, England, UK. andrew.thorley@imperial.ac.uk
Tetley
Teresa D
TD
D016207:Cytokines; D004847:Epithelial Cells / Q000378:metabolism; D004848:Epithelium / Q000503:physiopathology*; D006801:Humans; D008168:Lung / Q000166:cytology; D018384:Oxidative Stress; D010447:Peptide Hydrolases; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000503:physiopathology; D012907:Smoking / Q000009:adverse effects*; D006113:United Kingdom
D016207:Cytokines; D010447:Peptide Hydrolases