REVIEWS  ADVANCES IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) 

Minerva Pneumologica 2009 March;48(1):1-13

Copyright © 2009 EDIZIONI MINERVA MEDICA

language: English

Asthma and COPD: how similar are they?

Adapala R. K. ¹, Baptist A. P. ², Reddy R. C. ¹

¹ Department of Internal Medicine Division of Pulmonary and Critical Care Medicine University of Michigan Medical Center Ann Arbor, MI, USA 2 Department of Internal Medicine Division of Allergy and Clinical Immunology University of Michigan Medical Center Ann Arbor, MI, USA

Asthma and chronic obstructive pulmonary disease (COPD) are obstructive lung diseases characterized by inflammation and excess mucus production. They are typically quite distinct, however. Asthma is an eosinophil-dominant inflammation, driven by TH2 cytokines that most conspicuously affects the major airways, while COPD is a neutrophil- and macrophage-dominant inflammatory process, driven by TH1 cytokines, that has its greatest effects in the small airways and lung parenchyma. Neutrophils become prominent in severe asthma as well as in acute asthma exacerbations, however, while an influx of eosinophils is seen in acute exacerbations of COPD. These changes in the proportions of different inflammatory cells are accompanied by the appropriate shifts toward TH1 or TH2 cytokine patterns. The trigger for these changes remains unclear, however. The possibility that the recently discovered TH17 cells may play a role is intriguing, especially since they are essential for the upregulation of mucus production seen in both diseases. These cells and their cytokines may be especially important for the shift toward a more neutrophilic inflammation in asthma, since IL-17F, a cytokine isoform predominantly produced by these cells, has been shown to determine a neutrophilic rather than eosinophilic response to allergen challenge in a murine model of allergic airway disease. Significantly, levels of IL-17 are elevated in patients with severe asthma. The basis for the increased eosinophilia in acute COPD exacerbations requires further investigation, however. More broadly, the failure of inflammation to resolve, whether driven by TH17, TH1, or TH2 cells, remains the central enigma of these diseases.