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Pathophysiology of Exacerbations of Chronic Obstructive Pulmonary Disease

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 mediators—for 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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