The authors established that cigarette smoke increases airway epithelial platelet activating factor receptor (PAFr) expression and that PAFr is markedly up-regulated in the lungs of chronic obstructive pulmonary disease (COPD) patients. Crucially, PAFr is used by the two key bacterial species involved in chronic infection and acute exacerbations in COPD, that is, Streptococcus pneumoniae and Haemophilus influenzae, as a receptor for lung epithelial colonization. The cognate adhesin of PAFr, phosphorylcholine (ChoP), in the cell wall of these bacterial species may be a key effector that underpins host colonization. In this review, the authors evaluate the respective roles of PAFr and ChoP in the natural history of COPD and discuss the potential of the airway epithelial PAFr-bacterial ChoP interaction as a selective anti-infective target in COPD therapeutics.
Keywords: PAFr antagonist; airway epithelium; bacterial adhesion; inhaled corticosteroids; platelet activating factor receptor; pneumococcal infections.