Airborne pathogens represents a topic of great scientific relevance, especially considering the recent COVID-19 pandemic. Air pollutant such as Particulate Matter (PM) can in fact be associated with an increased incidence of respiratory viral diseases.1 To provide useful insights into the mechanisms by which PM could be involved into infection, we exposed human lung cells to fine PM (PM2.5) and SARS-CoV-2, in order to evaluate different particles cytotoxicological properties and the molecular pathways activated after 72 hours of treatment. We also explored the combined effects of PM2.5 and SARS-CoV-2, to verify the possibility that PM2.5 may play a role in facilitating SARS-CoV-2 infection. Results demonstrated that inflammation is the key process involved in the cell response to PM2.5 and viral particles, albeit with differences. Interestingly, the harmful effects are increased when SARS-CoV-2 and PM2.5 are combined. We also found that PM2.5 induces an over-expression of the angiotensin 2 converting enzyme (ACE2), a preferential entry for the viral particles into respiratory host cells.2 We then verified the possibility that a sub-chronic exposure to PM could induce a reduction of cellular defenses, thus making people more susceptible to infection. Cells were treated with PM2.5 for 72 hours, afterward SARS-CoV-2 was added for additional 2 and 24 hours. Data showed that pre-treatment with PM2.5 facilitates virus entry within the endosomal route already after 2 hours of exposure to SARS-CoV-2. We also demonstrated that the cells exposed to PM and successively treated with virus for 24 hours, respond with an intensified inflammatory state. Taken together, these results showed that PM2.5 appears to facilitate the virus entry in the lung, besides worsening the potency of the inflammatory response to viral infection. The times we are living in, solicit the urgency to carry out a more in-depth investigation, to provide useful elements for understanding the different mechanisms of action of bio-aerosols.
Marchetti, S., Gualtieri, M., Bragato, C., Colombo, A., Mantecca, P. (2023). AIR POLLUTION AND RESPIRATORY VIRAL DISEASES: A CASE STUDY ON THE EFFECT OF PM2.5 AND SARS-CoV-2 IN HUMAN LUNG CELLS. In ABSTRACT BOOK.
AIR POLLUTION AND RESPIRATORY VIRAL DISEASES: A CASE STUDY ON THE EFFECT OF PM2.5 AND SARS-CoV-2 IN HUMAN LUNG CELLS
S. Marchetti
Primo
;M. GualtieriSecondo
;C. Bragato;A. ColomboPenultimo
;P. ManteccaUltimo
2023
Abstract
Airborne pathogens represents a topic of great scientific relevance, especially considering the recent COVID-19 pandemic. Air pollutant such as Particulate Matter (PM) can in fact be associated with an increased incidence of respiratory viral diseases.1 To provide useful insights into the mechanisms by which PM could be involved into infection, we exposed human lung cells to fine PM (PM2.5) and SARS-CoV-2, in order to evaluate different particles cytotoxicological properties and the molecular pathways activated after 72 hours of treatment. We also explored the combined effects of PM2.5 and SARS-CoV-2, to verify the possibility that PM2.5 may play a role in facilitating SARS-CoV-2 infection. Results demonstrated that inflammation is the key process involved in the cell response to PM2.5 and viral particles, albeit with differences. Interestingly, the harmful effects are increased when SARS-CoV-2 and PM2.5 are combined. We also found that PM2.5 induces an over-expression of the angiotensin 2 converting enzyme (ACE2), a preferential entry for the viral particles into respiratory host cells.2 We then verified the possibility that a sub-chronic exposure to PM could induce a reduction of cellular defenses, thus making people more susceptible to infection. Cells were treated with PM2.5 for 72 hours, afterward SARS-CoV-2 was added for additional 2 and 24 hours. Data showed that pre-treatment with PM2.5 facilitates virus entry within the endosomal route already after 2 hours of exposure to SARS-CoV-2. We also demonstrated that the cells exposed to PM and successively treated with virus for 24 hours, respond with an intensified inflammatory state. Taken together, these results showed that PM2.5 appears to facilitate the virus entry in the lung, besides worsening the potency of the inflammatory response to viral infection. The times we are living in, solicit the urgency to carry out a more in-depth investigation, to provide useful elements for understanding the different mechanisms of action of bio-aerosols.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.