Brown, Jeremy S; (2024) The importance of airway IL-1β in patients with bronchiectasis. European Respiratory Journal , 64 (2) , Article 2400997. 10.1183/13993003.00997-2024.

Text Brown_ERJ-00997-2024 revised IL1 editorial JSBrown untracked.pdf Access restricted to UCL open access staff until 16 August 2025. Download (205kB)

Abstract

Airway inflammation drives both the development of bronchiectasis and results in the dominant clinical features. Many aetiologies of bronchiectasis, including previous infection, COPD, rheumatoid arthritis, allergic bronchopulmonary aspergillosis and toxic exposures, cause airway inflammation that damages the bronchial wall, which then allows chronic infection to be established. When bronchiectasis is caused by defects in airway immunity, although the disease maybe initiated by persistent bacterial bronchial infection, the inflammatory response to these bacteria then promotes worsening bronchiectasis through further damage to the bronchi. Once bronchiectasis is established, the degree of airway inflammation is closely correlated to the bacterial load in both stable disease and exacerbations [1–5]. Clinically, this airway inflammation is manifested by regular sputum production and increasing sputum purulence during exacerbations or with more severe disease [6], along with bronchial wall thickening, peribronchial consolidation and tree-in-bud changes seen on lung computed tomography scans. Overall, in patients with bronchiectasis, airway inflammation caused by bronchial infection is both a key influence on the clinical manifestations of the disease and can drive further disease progression.

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