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 participa te in the inflammatory process. However, the respective importance of these cells and their level of activation are difficult to quantitate because di sease phenotyping, and compartmentalization of inflammation and markers of inflammation in the lung, influence the obtained data and bias their interp retation. Bronchoscopic biopsies are typically obtained from larger, cartil aginous airways containing submucosal glands whereas the site of airflow ob struction in COPD is predominantly the membranous bronchiole, devoid of car tilage and submucosal glands. This makes it difficult to establish structur e-function relationships. The proportion of neutrophils has been reported t o increase in repeated induced sputum and bronchoalveolar lavage samples. T his observation suggests neutrophil recruitment into the airway is induced by the tests or sampling of different airway compartments in subsequent tes ts. There appears to be a good correlation between the proportions of eosin ophils in induced sputum and bronchoalveolar lavage fluid on the one hand a nd in airway tissue on the other. However, this is not the case for other i nflammatory cells, especially T lymphocytes, which are more numerous in air way tissue. Despite these inconsistencies, induced sputum, bronchoalveolar lavage, and bronchial biopsies can be used as markers of inflammation in CO PD as long as their limitations are recognized.