Infection and remodelling: a 21st century model of bronchiectasis?

Abstract

Non-cystic fibrosis bronchiectasis is defined according to morphological criteria as the permanent dilatation of bronchi. Numerous causes have been identified, with a common end-point of repeated, vicious cycles of infection, inflammation and airway structural changes [1]. There is a general belief that the incidence of bronchiectasis is falling, but this is poorly researched [1, 2]. When assessed, prevalence estimates vary widely between populations from 3.7 per 100,000 children in New Zealand to 52 per 100,000 adults in the USA [1]. Clinical descriptions of bronchiectasis made over 200 yrs ago by Rene Theophile Hyacinthe Laennec, the inventor of the stethoscope, vividly reflect the considerable associated morbidity: “This affection of the bronchia is always produced by chronic catarrh, or by some other disease attended by long, violent, and often repeated fits of coughing” [3]. The spectrum of bronchiectasis can range from mild, almost asymptomatic disease, through to disease showing accelerated loss of lung function and leading to death. Such decline of lung function in bronchiectasis is often associated with chronic colonisation by Pseudomonas aeruginosa , the occurrence of severe exacerbations, and evidence of systemic inflammation [1]. The British Thoracic Society clinical guidelines on bronchiectasis have recently been published [2]. A notable aspect of the guidelines was that much of the evidence cited had the designation of “level D” i.e. non-analytic studies ( e.g. case reports, case series) or expert opinion. In this issue of the European Respiratory Journal ( ERJ ), Martin et al. [4] provide much-needed thorough research of potential relevance to human bronchiectasis. Using epithelial cell lines, primary human epithelia and a murine model, they investigated the effects of Pseudomonas challenge, importantly assessing the effect of both lab- and patient-derived pathogens. The study showed that infection with P. …