Bronchiectasis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.
Overview
Bronchiectasis involves bronchi that are permanently dilated inflamed, and easily collapsible. This results in airflow obstruction and impaired clearance of secretions Cole's Cycle describes how infections and a defect in the host defense are factors for this disease. An immune response also plays a role in the pathogenesis, which involves neutrophils, lymphocytes, and macrophages.
Pathophysiology[1]
- Dilation of the bronchial walls results in airflow obstruction and impaired clearance of secretions
- The dilated areas interrupt normal air pressure of the bronchial tubes, causing sputum to pool inside the dilated areas instead of being pushed upward
- The pooled sputum provides an environment favorable to the growth of infectious pathogens
- The more infections that the lungs experience, the more damaged the alveoli in the lung become
- With more damage to the lung tissue, the bronchial tubes become more inelastic and dilated
- This creates a perpetual, destructive cycle
- The biopsies indicate that the infiltrate contains neutrophils, T lymphocytes and macrophages
- The sputum contains elastase, interleukin-8, tumor necrosis factor a (TNF-a), and prostanoids
Cole's Cycle[2]
- Also known as Cole's "vicious cycle hypothesis"
- The most widely known model of the development of bronchiectasis
- Impaired muco-ciliary clearance due to genetic susceptibility causes environmental insult
- Results in persistence of microbes in the sinobronchial tree
- The microbial infection causes chronic inflammation
- This results in tissue damage and impaired mucociliary motility
- This leads to more infection with a cycle of inflammation causing lung damage
- Two factors required for the development of this condition are persistent infection and a defect in host defense
Immune Response
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Schematic representation of a vicious circle of events which occurs during chronic bronchial infection. IL: interleukin; TNF: tumour necrosis factor; LT: leukotriene; MMP: matrix metalloproteinase
European Respiratory Journal
