22nd February 2024

Pathophysiology

The pathophysiology of bronchiectasis stems from two main processes: infectious insult and subsequent impaired drainage leading to airway obstruction.

The host immune response, led mainly through immune modulator cells (neutrophils) and elastases, in addition to oxidation radicals and inflammatory cytokines, leads to ulceration, inflammation and neovascularisation of airways. Other contributing factors include:

Neutrophil/Neutrophil elastase

The excess presence of neutrophil/neutrophil elastase has been noted in patients with features of bronchiectasis. Unopposed apoptosis, increased release of myeloperoxidase and phagocytosis have been characterised with stable bronchiectasis. Pregnancy-associated zone proteins (PZP) and intracellular neutrophil proteins are associated with infective exacerbation of bronchiectasis and indicate the presence of Pseudomonas aeruginosa. 

Vitamin D deficiency

Vitamin D has been correlated with exacerbation of bronchiectasis. Patients with Vitamin D deficiency are more likely to have Pseudomonas colonisation, worse exacerbations requiring hospitalisation and increased sputum expectancy.