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Role of Interleukin-8 in the Pathogenesis and Treatment of COPD

Antonino Di Stefano, PhD; Armando Capelli, MD; Claudio F. Donner, MD, FCCP
Author and Funding Information

Affiliations: Veruno, Italy
 ,  Dr. Di Stefano is Research Biologist, Dr. Capelli is Respiratory Physician, and Dr. Donner is Chief, Division of Pulmonary Disease, Salvatore Maugeri Foundation IRCCS, Scientific Institute of Veruno.

Correspondence to: Claudio F. Donner, MD, FCCP, Divisione di Pneumologia, Fondazione S. Maugeri, IRCCS, Istituto Scientifico di Veruno, Via per Revislate, 13, 28010 Veruno (NO), Italy; e-mail: cdonner@fsm.it



Chest. 2004;126(3):676-678. doi:10.1378/chest.126.3.676
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In the last decade, the role of inflammation and of proinflammatory cytokines in the pathogenesis of COPD has been extensively investigated. Studies1 performed in bronchial biopsy specimens and in the peripheral airways of COPD patients have shown that a mononuclear cell infiltration, consisting predominantly of T lymphocytes and macrophages, is prevalent in patients with mild disease, while neutrophils and macrophages have become the prevalent inflammatory cells in patients with more severe states of the disease. Although the role of neutrophils in the pathogenesis of COPD still has not been fully clarified, it is likely that neutrophil accumulation in the airways of patients with COPD is driven by an increased release of cytokines exerting a chemotactic effect on these cells. This pattern of inflammatory cell prevalence is accompanied by increased levels of intercellular adhesion molecule-1, macrophage inflammatory protein-1α, and interleukin (IL)-8 in the epithelium, and of endothelial adhesion molecule-1 in the submucosal endothelium of severely diseased patients,13 and by increased levels of phospho-signal transducer and activator of transcription-4, interferon-γ, and nuclear factor-κB in bronchial biopsy specimens from patients with mild-to-moderate disease.45 Total inflammatory cell infiltration was reported to be decreased in association with increased fibrotic modifications in the airways of patients with severe disease, compared to those with the mildest forms of COPD.1

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