Fine particulate matter PM2.5 and its constituent, hexavalent chromium induce acute cytotoxicity in human airway epithelial cells via inflammasome-mediated pyroptosis
Issued Date
2024-04-01
Resource Type
ISSN
13826689
eISSN
18727077
Scopus ID
2-s2.0-85188247685
Pubmed ID
38492761
Journal Title
Environmental Toxicology and Pharmacology
Volume
107
Rights Holder(s)
SCOPUS
Bibliographic Citation
Environmental Toxicology and Pharmacology Vol.107 (2024)
Suggested Citation
Moonwiriyakit A., Dinsuwannakol S., Sontikun J., Timpratueang K., Muanprasat C., Khemawoot P. Fine particulate matter PM2.5 and its constituent, hexavalent chromium induce acute cytotoxicity in human airway epithelial cells via inflammasome-mediated pyroptosis. Environmental Toxicology and Pharmacology Vol.107 (2024). doi:10.1016/j.etap.2024.104416 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/97757
Title
Fine particulate matter PM2.5 and its constituent, hexavalent chromium induce acute cytotoxicity in human airway epithelial cells via inflammasome-mediated pyroptosis
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Corresponding Author(s)
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Abstract
PM2.5-induced airway injury contributes to an increased rate of respiratory morbidity. However, the relationship between PM2.5 toxicants and acute cytotoxic effects remains poorly understood. This study aimed to investigate the mechanisms of PM2.5- and its constituent-induced cytotoxicity in human airway epithelial cells. Exposure to PM2.5 resulted in dose-dependent cytotoxicity within 24 h. Among the PM2.5 constituents examined, Cr(VI) at the dose found in PM2.5 exhibited cytotoxic effects. Both PM2.5 and Cr(VI) cause necrosis while also upregulating the expression of proinflammatory cytokine transcripts. Interestingly, exposure to the conditioned PM, obtained from adsorption in the Cr(VI)-reducing agents, FeSO4 and EDTA, showed a decrease in cytotoxicity. Furthermore, PM2.5 mechanistically enhances programmed pyroptosis through the activation of NLRP3/caspase-1/Gasdermin D pathway and increase of IL-1β. These pyroptosis markers were reduced when exposure to conditioned PM. These findings provide a deeper understanding of mechanisms underlying PM2.5 and Cr(VI) in acute airway toxicity.