Bronchiectasis pathophysiology

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Bronchiectasis Microchapters


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.


Bronchiectasis involves cycles of infections and inflammation that result in alveolar damage and inelastic dilated bronchi. Damage to the airway results in airflow obstruction and impaired clearance of secretions.


The following events summarize the pathophysiology of bronchiectasis:[1]

Cole's Cycle

The following events summarize Cole's cycle (Cole's "vicious cycle hypothesis"), which is the most widely known model of the development of bronchiectasis:[2]

  • Two factors are required for the development of bronchiectasis:
    • Persistent infection
    • Host defense derangement
  • Impaired mucociliary clearance due to the genetic susceptibility may cause environmental insult.
  • Insults result in persistence of microbes in the sinobronchial tree.
  • The microbial infection can cause chronic inflammation, which may result in tissue damage and impaired mucociliary motility.
  • Inflammation ensues more infection, which in turn ensues more inflammation.

Immune Response

The diagram below depicts the immune response for bronchiectasis:

Gross Pathology


  1. Morrissey BM (2007). "Pathogenesis of bronchiectasis". Clin Chest Med. 28 (2): 289–96. PMID 17467548.
  2. King PT (2009). "The pathophysiology of bronchiectasis". Int J Chron Obstruct Pulmon Dis. 4: 411–9. PMC 2793069. PMID 20037680.

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