Platelet activating factor receptor (PAFr) expression is increased in airways of COPD patients but is not attenuated by inhaled corticosteroid (ICS)

Introduction: Bacterial adhesion to airway epithlium is a prerequisite for colonization and infection that may be very relevant to COPD. Bacterial phosphorylcholine specifically binds to PAFr expressed by airway epithelium facilitating adherence and tissue invasion. We recently published that PAFr is upregulated in the epithelium of the proximal airways of current smokers and bronchial epithelial cells exposed to cigarette smoke extract demonstrated upregulation of Streptococcus pneumoniae adhesion. Evidently, ICS in COPD patients are associated with an increased risk of pneumococcal pneumonia. Objective: In this study we have investigated whether PAFr is upregulated in COPD and whether PAFr expression is affected by ICS. Methods: Cross-sectionally we evaluated PAFr expression in bronchial biopsies from 15 COPD patients who were current smokers (CCS), 12 COPD ex- smokers (CES), 16 smokers with normal lung function (NLFS) and 11 normal controls (NC) by immunostaining with anti-PAFr monoclonal antibody. We also analysed airway samples from a placebo controlled intervention study in COPD to assess the effect of ICS on PAFr expression. We employed computer-aided image analysis to quantify the percentage of epithelium stained for PAFr. Results: Significantly enhanced expression of PAFr was found in CCS (p<0.002) and CES (p<0.002), even more than in NLFS (p<0.03) when compared to NC. PAFr expression went up after ICS therapy, but this was not significant. Conclusion: PAFr is upregulated in smokers but especially in COPD. This pilot study indicated increased PAFr expression following ICS therapy and further work is warranted with larger cohort.