Mechanisms of immune dysfunction and bacterial persistence in non-cystic fibrosis bronchiectasis

James D. Chalmers, Adam T. Hill

    Research output: Contribution to journalArticlepeer-review

    141 Citations (Scopus)


    Bronchiectasis is a chronic inflammatory lung disease. The underlying cause is not identified in the majority of patients, but bronchiectasis is associated with a number of severe infections, immunodeficiencies and autoimmune disorders. Regardless of the underlying cause, the disease is characterised by a vicious cycle of bacterial colonisation, airway inflammation and airway structural damage. Inflammation in bronchiectasis is predominantly neutrophil driven. Neutrophils migrate to the airway under the action of pro-inflammatory cytokines such as interleukin-8, tumour necrosis factor-a and interleukin-1ß, all of which are increased in the airway of patients with bronchiectasis.Bacterial infection persists in the airway despite large numbers of neutrophils that would be expected to phagocytose and kill pathogens under normal circumstances. Evidence suggests that neutrophils are disabled by multiple mechanisms including cleavage of phagocytic receptors by neutrophil elastase and inhibition of phagocytosis by neutrophil peptides. Complement activation is impaired and neutrophil elastase may cleave activated complement from pathogens preventing effective opsonisation.Organisms also evade clearance by adapting to chronic infection. The formation of biofilms, reduced motility and the down-regulation of virulence factors are among the strategies used to subvert innate immune mechanisms.Greater understanding of the mechanisms underlying chronic colonisation in bronchiectasis will assist in the development of new treatments for this important disease.
    Original languageEnglish
    Pages (from-to)27-34
    Number of pages8
    JournalMolecular Immunology
    Issue number1
    Publication statusPublished - Aug 2013


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