Pathophysiology of exacerbations of chronic obstructive pulmonary disease.
Smokers with stable chronic obstructive pulmonary disease have a chronic inflammation of the entire tracheobronchial tree characterized by an increased number of macrophages and CD8 T lymphocytes in the airway wall and of neutrophils in the airway lumen. Exacerbations of chronic obstructive pulmonary disease are considered to reflect worsening of the underlying chronic inflammation of the airways, caused mainly by viral and bacterial infections and air pollution. During exacerbations, the inflammatory cellular pattern changes, with a further increase of eosinophils and/or neutrophils and various inflammatory mediators--for example, cytokines (tumor necrosis factor-alpha, RANTES [regulated upon activation normal T cell-expressed and secreted], and eotaxin-1), chemokines (CXCL5 [ENA-78], CXCL8), chemokine receptors (CCR3, CXCR1, and CXCR2), adhesion molecules (E-selectin and ICAM-1), and markers of oxidative stress (H(2)O(2) and 8-isoprostane, glutathione depletion). Worsening of inflammation is considered responsible for the deterioration of lung function and clinical status during exacerbations.
Papi
Alberto
A
Department of Clinical and Experimental Medicine, Centre of Research on Asthma and COPD, University of Ferrara, Italy. fabbri.leonardo@unimo.it
Luppi
Fabrizio
F
Franco
Francesca
F
Fabbri
Leonardo M
LM
D000397:Air Pollution; D001424:Bacterial Infections / Q000453:epidemiology; D016207:Cytokines / Q000502:physiology; D018450:Disease Progression; D004804:Eosinophils / Q000502:physiology; D006801:Humans; D009504:Neutrophils / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology; D029424:Pulmonary Disease, Chronic Obstructive / Q000382:microbiology / Q000503:physiopathology* / Q000821:virology; D012129:Respiratory Function Tests; D013183:Sputum / Q000382:microbiology; D014777:Virus Diseases / Q000453:epidemiology
D016207:Cytokines