Synergistic effects of PM2.5 and viral challenge on the modulation of antiviral defence and pro-inflammatory cytokines in HBECs in vitro

<bold>Background:</bold> The airway epithelium, which acts as a physical barrier to inhaled agents, is a major target for fine particulate matter (PM2.5) and respiratory viral infections. Rhinovirus (RV) infection has been identified as a major cause of acute asthma exacerbations, and studies have shown that PM2.5 and viral infections may act in synergy to aggravate airway inflammation. However, the mechanisms underlying the interaction of PM2.5 and viral infections remain unclear. <bold>Aim:</bold> To investigate the interaction between PM2.5 exposure and viral stimulus on human bronchial epithelial cells (HBECs) in vitro. <bold>Methods:</bold> HBECs were exposed to various concentrations of PM2.5 (10, 100 and 200 μg/ml) for 3, 6 and 24hrs or exposed 24h prior to stimulation with the RV infection mimic, Poly(I:C) (10 μg/ml), for 24h. Samples were analyzed with RT-qPCR for mRNA expression. <bold>Results:</bold> HBECs exposed to PM2.5 alone for 3, 6 and 24hrs dose-dependently increased the gene expression of IL-1β, IL-6 and IL-8 and decreased the expression of E-Cadherin. HBECs initially exposed to PM2.5 prior to Poly(I:C), resulted in further induction of IL-8 and IL-1β (P<.02) and reduced (P<.01) antiviral response including, IFN-β, IFN-λ and PRRs at 24h compared to Poly(I:C) alone. <bold>Conclusion:</bold> PM2.5 may impair barrier function in HBECs by reducing tight junction protein expression and inflammatory cytokine production. Additionally, PM2.5 can suppress viral-induced IFNs and PRRs expression, and increase bronchial epithelial inflammatory responses prior to viral infections. These findings shed new insights on the synergy between PM2.5 and viral infection, which is relevant to asthma exacerbation.