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.

中文翻译：

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在人类 3D 支气管上皮模型中，暴露于 PM2.5 可调节针对流感病毒感染的促炎和干扰素反应

流行病学研究表明，接触 PM 与流感病毒感染的严重程度呈正相关。然而，PM 破坏抗病毒防御的机制仍不清楚。从这个角度来看，本研究的目的是利用在气液界面生长的支气管 Calu-3 细胞系来评估 PM 对呼吸道上皮细胞抗病毒信号传导的影响。研究了感染流感病毒之前接触 PM 的情况以及同时接触情况。尽管病毒和颗粒之间似乎可能存在物理相互作用，但在共同暴露期间没有观察到 PM 对病毒复制的影响，尽管 IFN-β 释放的下调与 PM 暴露有关。然而，预暴露略微增加了病毒核蛋白的产生和促炎症反应。相反，粘病毒抗性蛋白 A (MxA)（一种由 IFN-β 诱导的干扰素刺激基因 (ISG)）的水平降低。因此，这些结果表明，预先暴露于 PM 可能会改变支气管上皮细胞的抗病毒反应，增加其对病毒感染的易感性。