Abstract

Neutrophils provide innate immune defence against microbes such as bacteria. Neutrophilic airway inflammation is a characteristic feature of chronic obstructive pulmonary disease (COPD) (Hogg et al., 2004), a condition that is commonly caused by cigarette smoking. Neutrophils activated by the inhalation of toxic particles contribute to the pathophysiology of COPD by secreting proteases that cause tissue destruction and by releasing mediators that promote airway inflammation. On the one hand, it could be therapeutically beneficial to reduce neutrophil activity in COPD lungs. On the other hand, one has to be careful about preserving anti-bacterial defence. This is particularly relevant for the subset of COPD patients who have persistent bacterial colonisation and/or acute bacterial exacerbations, often caused by nontypeable Haemophilus influenzae (NTHi) or Streptococcus pneumoniae (Desai et al., 2014).

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