The Proceedings of the American Thoracic Society 3:245-251 (2006)
© 2006 The American Thoracic Society
Pathophysiology of Exacerbations of Chronic Obstructive Pulmonary Disease
Alberto Papi,
Fabrizio Luppi,
Francesca Franco and
Leonardo M. Fabbri
Department of Clinical and Experimental Medicine, Centre of Research on Asthma and COPD, University of Ferrara, Ferrara; and Department of Oncology, Hematology, and Pneumonology, Section of Respiratory Diseases, University of Modena & Reggio Emilia, Modena, Italy
Correspondence and requests for reprints should be addressed to Leonardo M. Fabbri, M.D., Department of Respiratory Diseases, Via del Pozzo 71, 41100, Modena, Italy. E-mail: fabbri.leonardo{at}unimo.it
ABSTRACT
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 mediatorsfor example, cytokines (tumor necrosis factor- , 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 (H2O2 and 8-isoprostane, glutathione depletion). Worsening of inflammation is considered responsible for the deterioration of lung function and clinical status during exacerbations.
Key Words: airway chemokines cytokines inflammation leukocytes
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Copyright © 2006 by the American Thoracic Society.
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