Infectious mechanisms regulating susceptibility to acute exacerbations of COPD

Acute exacerbations of COPD (AECOPD) are defined by clinical criteria, outlined in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines [1]. These include an acute increase in one or more of the following cardinal symptoms, beyond day to day variability: dyspnea, increased frequency or severity of cough and increased volume or change in character of sputum, which represent an acute increase in airway inflammation. The role of infection in the pathogenesis of COPD, acute exacerbation and disease progression has been a clinical and research question for many years, and the pendulum has swung from infection as a major cause of acute exacerbation and COPD (British Hypothesis) [2], to infection as an unrelated epiphomenon in acute exacerbation [3-5], and back again to infection as integral in the development of AECOPD and likely an important contributor to COPD progression [6-19]. Upwards of 80 % of AECOPD are driven by infectious stimuli, with 40-50 % associated with bacterial infection and 30-50 % associated with acute viral infection, with some exacerbations having dual bacterial and viral causation [20]. Much of the advancement in our understanding of the role of infection is AECOPD is due to the advancement of clinical and research tools that have allowed researchers to accurately characterize the microbial pathogens, and better understand the host-pathogen interactions (Table 1).