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Effects of Particulate Matter on SARS-CoV-2 Induced Antiviral Responses in Human Nasal Epithelial Cells
American Journal of Respiratory and Critical Care Medicine ; 203(9), 2021.
Article in English | EMBASE | ID: covidwho-1277737
ABSTRACT
Rationale We have previously shown that particulate air pollution hampers antiviral responses to influenza virus in human nasal epithelial cells (hNECs) and that exposure to particulate matter from woodsmoke alters antiviral response to live attenuated influenza virus in the nasal epithelium. In 2020, more than 10 million acres of U.S. land burned in record-breaking wildfires and epidemiological data has indicated that increased exposure to particulate and gaseous air pollution is correlated with increased COVID-19 cases. Additionally, SARS-CoV-2 has demonstrated tropism for nasal epithelium more so than other airway regions. Hence, interactions between particulate air pollutants and antiviral responses in hNECs is likely regulating susceptibility to SARS-CoV-2 infections.

Methods:

Primary hNECs from 13 healthy donors (6 male, 7 female) were cultured at air liquid interface for six weeks, at which point ciliation and mucus production could be observed. Cells from 3 males and 3 females were exposed to particulate matter from diesel exhaust, woodsmoke from flaming eucalyptus, or woodsmoke from flaming red oak at 22 μg/cm2 for 2h. These cells were subsequently infected with SARS-CoV-2 and samples were collected at 0h, 24h, and 72h post infection for analysis of viral replication, expression of antiviral host defense markers, and biomarkers of inflammation.

Results:

Pilot data revealed that exposure of hNECs to 22 μg/cm2 of diesel exhaust particles for 2h decreased mRNA expression of genes related to antiviral responses, such as IRF1 and IRF3, DDX58, and CXCL10, but increased IL6 expression. However, hNEC exposure to diesel exhaust also decreased mRNA expression of ACE2 and TMPRSS2, two genes which provide crucial machinery for SARS-CoV-2 viral entry.

Conclusions:

Based on these pilot data we hypothesize that exposure to particulate air pollution from diesel exhaust and woodsmoke will increase viral load and severity of infection in hNECs infected with SARS-CoV-2. Ongoing analysis of viral replication, antiviral and inflammatory gene expression will further elucidate potential effects of different particulate air pollutants on SARS-CoV-2 infections.

Full text: Available Collection: Databases of international organizations Database: EMBASE Type of study: Experimental Studies Language: English Journal: American Journal of Respiratory and Critical Care Medicine Year: 2021 Document Type: Article

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Full text: Available Collection: Databases of international organizations Database: EMBASE Type of study: Experimental Studies Language: English Journal: American Journal of Respiratory and Critical Care Medicine Year: 2021 Document Type: Article