Introduction

Extracellular ATP in the purinergic pathway is involved in COPD pathogenesis and may contribute to chronic inflammation. We assess CD73 ectonucleotidase expression in COPD patients with different clinical phenotypes and its correlation with inflammatory markers.

Matherial and methods

Prospective observational study in stable COPD patients categorized into exacerbators (?2 exacerbations/year) and non-exacerbators. Blood and sputum samples were collected in stable patients and during exacerbations. ELISA determined CD73 expression and cytokines (IL6, IL8, IL13, TNF-?).

Results

47 patients were included, 24 being exacerbators (68±8 years). Exacerbators had higher obstruction (FEV1 43.8±16%vs61.4±19%,p<0.001) and symptoms (mMRC 2[2-2]vs[1-3],p<0.001). Non-exacerbators had higher eosinophils and cytokine levels in serum (p>0.05). CD73 expression in blood and sputum didn't differ between COPD groups. During exacerbations, serum CD73 decreased alongside eosinophils, while inflammatory markers and cytokines increased (p<0.05 for IL6, neutrophils, CRP and fibrinogen). Sputum CD73 showed a tendency to increase with higher eosinophils. No correlation was found between CD73 and inflammatory markers.

Conclusions

Inflammatory profile in COPD patients doesn't vary by exacerbator phenotype. However, the assotiation between CD73 and eosinophilia implies potential purinergic pathway involvement in eosinophilic inflammation.