ArticleScientific reports2024
Oxidized phospholipid and transcriptomic signatures of THC-related vaping associated lung injury.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Preclinical models of COPD: a state of the art review.The European respiratory journal · 2026Review
- Chaiyin Granules Improve Acute Lung Injury by Regulating Gut Microbiota and Unsaturated Fatty Acid Mediated Wnt/β-Catenin Signaling Pathway.Journal of immunology research · 2026Article
- Childhood Interstitial Lung Disease (chILD) Associated With Toxic Chemical Inhalation Exposures: A State-of-the-Art Review.Pediatric pulmonology · 2025Review
- Clinical Impact of Vaping.Toxics · 2025Review
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Authors and funding
25 authors.
Funding
Abstract
E-cigarette/vaping-associated lung injury (EVALI) is strongly associated with vitamin E acetate and often occurs with concomitant tetrahydrocannabinol (THC) use. To uncover pathways associated with EVALI, we examined cytokines, transcriptomic signatures, and lipidomic profiles in bronchoalveolar lavage fluid (BALF) from THC-EVALI patients. At a single center, we prospectively enrolled mechanically ventilated patients with EVALI from THC-containing products (N = 4) and patients with non-vaping acute lung injury and airway controls (N = 5). BALF samples were analyzed by Luminex multiplex assay, RNA sequencing, and mass spectrometry. After treating BEAS-2B lung epithelial cells with vaping and non-vaping BALF, LDH release was quantified. THC-EVALI BALF had significant increases in IFNγ, CCL2, CXCL5, and MMP2 relative to non-vaping patients. RNA sequencing showed enrichment for biological oxidation, glucuronidation, and fatty acid metabolism pathways. Oleic acid and arachidonic acid metabolites were increased in THC-EVALI, as were oxidized phosphatidylethanolamines (PE) such as PE(38:4). THC-EVALI BALF induced more LDH release compared to BALF from non-vaping patients. Thus, THC-EVALI is characterized by altered phospholipid composition, accumulation of lipid oxidation products, and increased pro-inflammatory mediators that may contribute to epithelial cell death. These findings serve as a framework to study novel oxidized phospholipids implicated in the pathogenesis of EVALI.
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