Abstract

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.