Resolvin D1 reduces the inflammatory response to rhinovirus infection in COPD bronchial epithelial cells

<bold>Background:</bold> COPD exacerbations (AECOPD) caused by viruses are associated with prolonged symptoms, impaired recovery, and more severe disease. Specialised pro-resolving mediators (SPMs) such as Resolvin D1 (RvD1) are lipid mediators that promote resolution of airway inflammation following a respiratory infection. <bold>Objectives:</bold> Using bronchial epithelial cells from COPD patients (COPD-BECs) infected with Human Rhinovirus-16 (RV16), we investigated how RvD1 affected pro-inflammatory cytokines release, Rhinovirus (RV) load and interferon stimulated genes (ISGs). <bold>Methods:</bold> We treated COPD-BECs (patient n=6) with vehicle or exogenous 1nM RvD1 30 minutes pre-infection with RV16, and again 24 hours post-infection to simulate both prophylactic and post-AECOPD treatment response respectively. We collected supernatant at 0,6,24,48 and 72h and used Mesoscale Discovery Platform to measure concentration of IFN-α2a, IFN-β, IFN-γ, IL-1β, IL-6, IL-8, IL-10, IL-29/IFN-λ1, and TNF-α. We measured RV load, 18S and ISGs (OAS, MxA, Viperin) in cell lysates by qPCR. <bold>Results:</bold> Culturing RV16 infected COPD-BECs with RvD1 at 24h exhibited significantly reduced IL-6 (197 pg/mL vs 722 pg/mL p=0.039) and IL-1β (266 pg/mL v 511 pg/mL p=0.048) relative to vehicle but interferon release was not inhibited. RvD1 exposure did not reduce RV viral load or ISG expression. <bold>Conclusion:</bold> RvD1 reduced the inflammatory response to RV infection in COPD-BECs without impairing interferon response. RvD1 may have therapeutic potential in ameliorating the inflammatory airway response to RV in AECOPD to enhance exacerbation recovery.