Repeated exposures to PM2.5 alter the mitochondria and the influenza-mediated interferon response in an air-liquid interface bronchial epithelium.

Humans are exposed to various contaminants, including fine atmospheric particles (PM2.5) and respiratory viruses. Epidemiological studies have demonstrated a positive association between exposure to PM2.5 and the severity of viral infections, including those caused by influenza viruses. Nevertheless, there is a paucity of in vitro studies investigating the underlying mechanisms, especially in the context of repeated exposures to PM2.5, which more realistically reflect human exposure. This study aimed to perform repeated exposures to PM2.5 collected in Paris on an in vitro bronchial epithelium model at the air-liquid interface (ALI) prior to infection with influenza A virus (IAV), and to assess modulations of antiviral responses. This work firstly demonstrated particle internalisation and a sustained pro-inflammatory response during repeated exposures to PM2.5. Repeated exposures to PM2.5 prior to IAV infection revealed a downregulation of the interferon (IFN) pathway without modulation of the pro-inflammatory response. Furthermore, mitochondrial dysfunction was observed following repeated PM2.5 exposures, as well as an accumulation of autophagic vesicles and p62 protein. This suggests the involvement of mitochondrial alteration and/or blockage of autophagic flux in the modulation of the IFN signalling pathway, and warrants further investigation.