Exposure to PM modulate the pro-inflammatory and interferon responses against influenza virus infection in a human 3D bronchial epithelium model.

Epidemiological studies showed a positive association between exposure to PM and the severity of influenza virus infection. However, the mechanisms by which PM can disrupt antiviral defence are still unclear. From this perspective, the objective of this study was to evaluate the effects of PM on antiviral signalling in the respiratory epithelium using the bronchial Calu-3 cell line grown at the air-liquid interface. Pre-exposure to PM before infection with the influenza virus was investigated, as well as a co-exposure. Although a physical interaction between the virus and the particles seems possible, no effect of PM on viral replication was observed during co-exposure, although a downregulation of IFN-β release was associated to PM exposure. However, pre-exposure slightly increased the viral nucleoprotein production and the pro-inflammatory response. Conversely, the level of the myxovirus resistance protein A (MxA), an interferon-stimulated gene (ISG) induced by IFN-β, was reduced. Therefore, these results suggest that pre-exposure to PM could alter the antiviral response of bronchial epithelial cells, increasing their susceptibility to viral infection.