Bronchial inflammation in alpha-1-antitrypsin deficiency
Abstract
Chronic bronchitis was first recognised as a disabling disorder in 1808. It is often a feature of chronic obstructive pulmonary disease, and recent studies have shown that the neutrophil and in particular neutrophil elastase, released by activated neutrophils, is implicated in the pathogenesis of chronic bronchitis including the facilitation of bacterial colonisation. The degree of neutrophil influx has been shown to be associated, not only with worse lung function, but also the rate of progression of airflow obstruction. Many patients with chronic bronchitis are colonised with bacteria in the stable clinical state but it is not known how this affects upper airways inflammation, disease progression, frequency of exacerbations, or quality of life. Secretory leukoprotease inhabitor is thought to be the most critical anti-elastase in the upper airways whereas alpha-1-antitrypsin is thought to be less important, although more important at the alveolar level protecting against the development of emphysema. Patients with homozygous PiZ alpha-1-antitrypsin deficiency have decreased circulating (15-20% normal) and alveolar concentrations of alpha-1-antitrypsin which facilitate the development of early onset and rapidly progressive emphysema. About 30-40 % of these patients also have chronic bronchitis although the nature of the upper airways inflammation has not been studied. There have been few studies assessing the complex interplay of inflammatory cells and appropriate mediators…
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