Chronic obstructive pulmonary disease - Inflammation of small airways and lung parenchyma

Currently available information suggests that cigarette smoke-induced lung inflammation has a pathogenic role in the development of COPD. Neutrophils, eosinophils, alveolar macrophages, and lymphocytes all appear to participate in the inflammatory process. However, the respective importance of these cells and their level of activation are difficult to quantitate because disease phenotyping, and compartmentalization of inflammation and markers of inflammation in the lung, influence the obtained data and bias their interpretation. Bronchoscopic biopsies are typically obtained from larger, cartilaginous airways containing submucosal glands whereas the site of airflow obstruction in COPD is predominantly the membranous bronchiole, devoid of cartilage and submucosal glands. This makes it difficult to establish structure-function relationships. The proportion of neutrophils has been reported to increase in repeated induced sputum and bronchoalveolar lavage samples. This observation suggests neutrophil recruitment into the airway is induced by the tests or sampling of different airway compartments in subsequent tests. There appears to be a good correlation between the proportions of eosinophils in induced sputum and bronchoalveolar lavage fluid on the one hand and in airway tissue on the other. However, this is not the case for other inflammatory cells, especially T lymphocytes, which are more numerous in airway tissue. Despite these inconsistencies, induced sputum, bronchoalveolar lavage, and bronchial biopsies can be used as markers of inflammation in COPD as long as their limitations are recognized.