The inflammatory effector cell pattern in asthma and chronic obstructive pulmonary disease - what is it good for?

philic overlap observed between asthma and COPD has not yet been conclusively understood. Several reasons may account for overlapping features of asthma and COPD. First, asthma and COPD are common conditions affecting between 5 and 15% of the population each. Therefore, overlap is likely to occur by chance alone. Second, the two conditions may share common origins or risk factors, such as respiratory infections or smoking, leading to epigenetic alterations with different inflammatory patterns [1] . Third, the predominance of neutrophils or eosinophils observed in either condition may represent an epiphenomenon with little pathogenic or diagnostic relevance. The predominance of a given effector cell may simply be due to comorbidity, exogenous factors or treatment, such as corticosteroids, which are known to favor an increase in neutrophils while reducing the number of eosinophils [5] . A new study by Bafadhel et al. [6] published in this issue of Respiration uses a different approach to look at the overlap of asthma and COPD in respect to inflammation. First, the report explores airway inflammation as well as cytokine and chemokine expression in stable adult asthma and COPD patients using a novel two-step sputum processing method with dithio threitol supernatants and cytospin preparations, allowing analysis of a broad spectrum of cytokines previously not accessible. In addition, sputum neutrophils were significantly lower in mild asthma compared to moderate/severe disease whereas sputum eosinoThe two obstructive airway diseases bronchial asthma and chronic obstructive pulmonary disease (COPD) represent major global causes of disability and death. Asthma is commonly considered an allergic disease that develops in the first decade of life and is characterized by the presence of reversible airflow obstruction. In contrast, COPD develops later in life, is related to tobacco smoking and characterized by the presence of incompletely reversible or irreversible airflow obstruction as well as by accelerated lung function decline. However, it has long been recognized that asthma and COPD are heterogeneous and may show a considerable overlap in respect to clinical presentation, lung function, response to treatment and certain features of the underlying inflammation [1] . In respect to the associated inflammation, two major patterns have been defined based on the predominance of eosinophils or neutrophils detected in sputum, bronchoalveolar space and airway tissue. While an eosinophilic pattern can usually be found in asthma and is associated with increased serum immunoglobulin E concentration [2] , the neutrophilic pattern is preferentially observed in severe manifestations of the disease. In contrast, COPD is associated with a neutrophilic pattern whereas the presence of eosinophils indicates recurrent infections and accelerated lung function decline [3, 4] . Although several hypotheses have been proposed to explain the variable presence of the two inflammatory effector cell types, the nature of the eosinophilic/neutroPublished online: November 22, 2011