Pathogenesis of inflammation and repair in advanced COPD.
Chronic obstructive pulmonary disease is characterized by an abnormal persistent inflammatory response to noxious environmental stimuli, most commonly cigarette smoke. Although cigarette smoking elicits airway inflammation in all of those who smoke, persistent inflammation and clinically significant COPD occurs in only a minority of smokers. The pathogenesis of COPD involves the recruitment and regulation of neutrophils, macrophages, and lymphocytes to the lung, as well as the induction of oxidative stress, all of which result in lung parenchymal destruction and airway remodeling. Recent research has generated a greater understanding of the mechanisms responsible for COPD development, including new concepts in T cell biology and the increasing recognition that the processes governing lung cell apoptosis are upregulated. We are also starting to understand the reasons for continued inflammation even after smoking cessation, which accelerates the rate of lung function decline in COPD. Herein we review our current knowledge of the inflammatory pathways involved in COPD pathogenesis, as well as newer concepts that have begun to unfold in recent years.
Cornwell
William D
WD
Fels Institute for Cancer Research and Molecular Biology, Center for Substance Abuse Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Kim
Victor
V
Song
Changcheng
C
Rogers
Thomas J
TJ
D000818:Animals; D017209:Apoptosis; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D008168:Lung / Q000473:pathology; D008173:Lung Diseases, Obstructive / Q000503:physiopathology; D018384:Oxidative Stress; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology*; D012907:Smoking / Q000009:adverse effects; D016540:Smoking Cessation; D015854:Up-Regulation