Particulate matter exposure potentiates SARS-CoV-2 delta variant infection by suppressing epithelial antiviral responses
Issued Date
2026-01-01
Resource Type
eISSN
22352988
Scopus ID
2-s2.0-105027885584
Pubmed ID
41561095
Journal Title
Frontiers in Cellular and Infection Microbiology
Volume
15
Rights Holder(s)
SCOPUS
Bibliographic Citation
Frontiers in Cellular and Infection Microbiology Vol.15 (2026)
Suggested Citation
Kongsomros S., Paha J., Prasara-a P., Visamol S., Techapichetvanich P., Jiso A., Uppakara K., Morrow A.L., Thorman A.W., Chutipongtanate S., Khemawoot P., Thitithanyanont A. Particulate matter exposure potentiates SARS-CoV-2 delta variant infection by suppressing epithelial antiviral responses. Frontiers in Cellular and Infection Microbiology Vol.15 (2026). doi:10.3389/fcimb.2025.1694050 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/114663
Title
Particulate matter exposure potentiates SARS-CoV-2 delta variant infection by suppressing epithelial antiviral responses
Corresponding Author(s)
Other Contributor(s)
Abstract
Introduction: Airborne particulate matter (PM), particularly fine (PM<inf>2.5</inf>) and coarse (PM<inf>10</inf>) particles, is a major environmental health concern linked to increased respiratory morbidity and mortality. During the COVID-19 pandemic, epidemiological studies suggested that PM exposure may worsen SARS-CoV-2 infection outcomes; however, cellular mechanisms underlying this association remain incompletely understood. Here, we investigated how pre-exposure to PM<inf>2.5</inf> and PM<inf>10</inf> impacts SARS-CoV-2 infection dynamics in Calu-3 human epithelial cells. Methods: Calu-3 cells were pre-exposed to PM for 72 h prior to infection with either the wild-type Wuhan strain or the more virulent Delta variant for additional 48 h. Viral infection, receptor expression, apoptosis and cytokine responses were assessed. Results: PM<inf>10</inf>, but not PM<inf>2.5</inf>, enhanced Delta variant infection, increasing the proportion of infected cells by 13.7% and viral titers by 2.6-fold compared with controls. This enhancement was not attributable to changes in ACE2 receptor expression or viral entry efficiency but instead impaired antiviral defenses. PM10 pre-exposure suppressed apoptosis and reduced the expression of pro-inflammatory cytokines including IFN-γ, IP-10, and TNF-α during Delta infection. Discussion: These findings suggest that PM<inf>10</inf> compromise epithelial antiviral response by dampening apoptotic cell clearance and inflammatory responses, thereby creating a cellular condition more permissive to viral replication. Our study provides a mechanistic basis by which particulate air pollution may amplify SARS-CoV-2 pathogenicity in a variant-specific manner. These results underscore further validation in physiologically relevant systems and highlight the potential public health implications of air pollution during viral pandemics.