AKL3 - Chronic obstructive pulmonary disease (COPD) is characterized by an accelerated decline in FEV1 (forced expiratory volume in 1 second) with age. The most important cause of COPD is cigarette smoking, and smoking cessation is the only intervention that has been shown to slow decline in lung function, although only small numbers of patients with COPD manage to quit smoking. It is now recognized that COPD is associated with chronic inflammation both in the airways and in the lung parenchyma and airway inflammation has been related to the degree of airway obstruction, with an increased inflammatory process with worsening COPD.
 
Mucous hypersecretion is a hallmark of chronic airway diseases, including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis: Goblet cell hyperplasia and persistence are characteristic pathologic features. In asthmatics, 20–25% of airway epithelial cells are goblet cells, even in mild disease. All of these diseases have distinct aetiologies and different inflammatory responses that drive mucous hypersecretion. Airway mucus is a complex mixture of secretory products that provides a multifaceted defence against pulmonary infection. Mucus contains antimicrobial peptides such as defensins and enzymes such as lysozyme.
 
In asthma, inflammation appears to be mediated by allergen-specific Th2 cells, leading to eosinophilia, while in COPD, the inflammatory response is neutrophilic and may be induced by infection or components in cigarette smoke. Controlling inflammation is at the root of treatment through the use of corticosteroids and/or antibiotics, yet despite therapy, airway obstruction remains the cause of morbidity and mortality.
 
Mucous secretions in the airways in asthma and COPD appear to be a major cause of airway obstruction, ventilation-perfusion mismatching, and hypoxemia, leading to wheezing and dyspnoea. (Cohn L, Mucus in chronic airway diseases: sorting out the sticky details, J. Clin. Invest. 116:306-308, 2006)
 
Given the high prevalence of COPD, it may be worth defining a balance point that separates effective and pathologic mucous production.
 
Can and should we be doing more to control mucus? This then begs the question: is it possible to reduce airway obstruction in chronic lung disease by enabling excessive production of mucous to return to normal homeostatic levels?
 
AKL III offers a potential way to limit mucous production and improve lung function. Please contact us for further information.