Introduction Patients with Chronic Obstructive Pulmonary Disease (COPD) experience intermittent exacerbations. The frequency of exacerbations varies amongst patients but the ‘Frequent Exacerbator’ appears to be an independent disease phenotype. As frequent exacerbations are associated with more rapid lung function decline, a validated biomarker is needed to identify those susceptible, prompting rigorous medical treatment and aiding selective recruitment to clinical trials. Pulmonary and Activation-Regulated Chemokine (PARC/CCL18) is a plausible biomarker based on previous reports in other respiratory diseases, making it worthy of study in COPD.

Methods PARC was measured using ELISA in serum samples from 115 patients enrolled in The London COPD cohort, including 44 paired samples taken at baseline and exacerbation (pre-treatment). PARC was assessed with relation to exacerbation frequency and other inflammatory markers.

Results The study cohort comprised of 77 males, 34 current smokers, mean age 69.6 years (SD 9.1), FEV₁ 1.13 (0.47) l (45.3 (18.0)% predicted), baseline PARC concentration 124 ng/ml (40.4), median (IQR) exacerbation frequency 1.8/year (0.6–3.0). Higher PARC concentration was associated with more frequent exacerbations (r=0.22, p=0.035). PARC was not related to age, sex, BMI, disease severity (FEV₁), or smoking pack years (all p>0.05). Significantly lower PARC concentrations were found in current smokers compared to ex-smokers, 112 ng/ml vs 130 ng/ml respectively (p=0.036). PARC did not change from baseline to exacerbation (131 ng/ml vs 125 ng/ml, p=0.256), and the correlation between PARC in the two states was highly significant (r=0.53, p<0.0001). PARC was related to baseline CRP (r=0.28, p=0.013) and blood eosinophil count (r=0.39, p=0.001), with no significant associations at exacerbation, and no relationship with neutrophils or total white blood cell count.

Conclusion A relationship has been demonstrated between serum PARC concentration and exacerbation frequency in patients with COPD. Correlations between PARC, eosinophils and CRP indicate that this biomarker may identify a subset of patients with a particular inflammatory profile, suggesting specific treatment options. Further work should be carried out to explore the relevance of PARC as a biomarker in the COPD population.