The increasing prevalence of inflammatory lung disease is becoming a major heath
burden. Chronic inflammation is a key feature of asthma, chronic obstructive pulmonary disease
(COPD) and cystic fibrosis. These patients are prone to bacterial pathogens that contribute to
disease worsening. The reasons for this are unclear but may reflect defective pathogen clearance by
alveolar macrophages. For example, alveolar macrophages from patients with COPD have a educed
capacity to phagocytose bacteria and hence promote pulmonary bacterial colonisation. In cystic
fibrosis macrophages are also defective in removing bacteria and this coupled with reduced
acidification of the phagosome implies that macrophages contribute to ineffective bacterial uptake
and subsequent killing. Bacteria can also employ diverse strategies to subvert the macrophage
phagocytic pathway. For example, the capsule of Streptococcus pneumoniae prevents opsonisation
by complement proteins and therefore is not removed efficiently by macrophages. Understanding
the mechanisms underlying exacerbations of lung diseases will provide novel treatment strategies
that will be of benefit for the patients in the short-term but could also prevent the acceleration of the
disease process that is often associated with frequent exacerbations and ultimately improve the
quality of life for patients already living with debilitating disease.
