Primary Causes & Pathophysiology
Bronchiectasis follows Cole vicious cycle (self-reinforcing loop) of poor clearance, infection and inflammation. Damaged cilia (hair-like movers) and thick mucus cut clearance. Bacterial enzymes and neutrophil elastase (white cell enzyme) destroy elastin (wall protein) and cartilage (support tissue). Weak walls dilate irreversibly (permanently widen) and pool mucus. Pooling sustains biofilms (germ layers) and triggers flare-ups with further injury.
Severe infection destroys wall support and impairs clearing, starting a cycle of infection and dilation
Faulty salt transport dehydrates mucus and blocks clearing, causing chronic infection and wall breakdown
Genetic cilia failure prevents mucus propulsion, causing retention, infection and dilation
Low antibody output allows recurrent bacterial infection that injures walls and remodels airways
Mould allergy triggers inflammation and mucus plugging that damages central airways
Chronic bronchitis impairs clearing and promotes germ colonisation with dilated remodelling
Persistent mycobacteria drive granulomatous (lumpy immune) inflammation with wall destruction
Systemic immune dysregulation causes small airway inflammation with recurrent infection
Blocked segment traps mucus beyond the block, causing post-obstructive infection and local dilation