Extrait

Chronic obstructive pulmonary disease (COPD) is a long-term multifaceted inflammatory disease state that consists pathologically of chronic bronchitis, small airways disease and emphysema, which may occur alone or together in varying proportion [Fletcher, 1984]. In exacerbations of COPD, there are increases in neutrophils and eosinophils in sub-epithelial tissue and sputum [Saetta, 1994; Zhu, 2000, Hogg 2005]. The worldwide/local guidelines emphasize the functional consequences of the disease and the fundamental underlying inflammatory process, defining COPD, as “an inflammatory disease characterised by progressive development of airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases”. Exacerbations of COPD impose a substantial burden on health-care systems worldwide; they are a major cause of morbidity, mortality, and reduced health status. COPD exacerbations are associated with increased airway and systemic inflammation and physiological changes, especially the development of hyperinflation. They are triggered mainly by respiratory viruses and bacteria, which infect the lower airway and increase airway inflammation [Wedzicha 2007]. Taken together with the existing in vitro data on virus-induced inflammation in airway and inflammatory cells from COPD patients in overseas studies, there is a sound rationale for the presence of increased inflammation in cells taken from Japanese COPD patients. Then the primary objective of the study is to demonstrate that bronchial cells from Japanese patients with COPD exhibit increased inflammatory responsiveness compared to smoking and non-smoking controls.

Critère d'inclusion

• Lung Injury, Acute and Respiratory Distress Syndrome, Adult

Liens

• gsk