ArticleJournal of asthma and allergy2021
PM2.5 Aggravated OVA-Induced Epithelial Tight Junction Disruption Through Fas Associated via Death Domain-Dependent Apoptosis in Asthmatic Mice.
Article in Journal of asthma and allergy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting Tight Junction Proteins to Restore Airway Epithelial Barrier Function in Asthma.Current allergy and asthma reports · 2026Review
- Article
- PM2.5 induces lung injury via mtDNA-cGAS-STING-mediated macrophage M1 polarization.Frontiers in pharmacology · 2026Article
- PM2.5 as a driver of human health disorders: insights from the regulated cell death pathways.Military Medical Research · 2026Review
- CC16 alleviates PM2.5-induced airway inflammation in asthmatic mice by targeting the E-cadherin-mediated ferroptosis regulatory axis.Current research in toxicology · 2026Article
- ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo.Journal of inflammation (London, England) · 2025Article
- Eosinophil-derived interleukin-24 compromises epithelial integrity and aggravates airway remodeling in mouse models of allergic asthma.Nature communications · 2025Article
- Benzo[a]pyrene aggravated ovalbumin‑induced epithelial tight junction disruption via ROS driven‑NLRP3/Caspase‑1 signaling pathway in asthmatic mice.International journal of molecular medicine · 2025Article
- Fine Particulate Matter (PM2.5) Disrupts Intestinal Barrier Function by Inducing Oxidative Stress and PI3K/AKT-Mediated Inflammation in Caco-2 Cells.International journal of molecular sciences · 2025Article
- Specific Ambient PMEnvironmental science & technology · 2025Article
- Article
- METTL3-driven mFrontiers in immunology · 2025Article
- Fine particulate matter 2.5 induces susceptibility to Pseudomonas aeruginosa infection via expansion of PD-L1Respiratory research · 2024Article
- Per- and poly-fluoroalkyl substances (PFAS) effects on lung health: a perspective on the current literature and future recommendations.Frontiers in toxicology · 2024Review
- Programmed Cell Death in Asthma: Apoptosis, Autophagy, Pyroptosis, Ferroptosis, and Necroptosis.Journal of inflammation research · 2023Review
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExposure to air pollutants cause exacerbation of asthma, but the experimental evidence and the mechanisms still need to be collected and addressed.
methodsAsthma model was constructed by ovalbumin (OVA) combined with or without airborne fine particulate matter 2.5 (PM2.5) exposure. Lung sections were stained by hematoxylin-eosin staining (H&E) and Masson's trichrome. RNA-seq and gene set enrichment analysis (GSEA) was performed to identify the key pathway. TdT mediated dUTP Nick End Labeling (TUNEL) assay, real-time qPCR, Western blot, immunofluorescence and lentivirus transfection were applied for mechanism discovery.
resultsIn this study, we found PM2.5 aggravated airway inflammation in OVA-induced asthmatic mice. RNA-seq analysis also showed that epithelial mesenchymal transition (EMT) was enhanced in OVA-induced mice exposed to PM2.5 compared with that in OVA-induced mice. In the meantime, we observed that apoptosis was significantly increased in asthmatic mice exposed to PM2.5 by using GSEA analysis, which was validated by TUNEL assay. By using bioinformatic analysis, Fas associated via death domain (FADD), a new actor in innate immunity and inflammation, was identified to be related to apoptosis, EMT and tight junction. Furthermore, we found that the transcript and protein levels of tight junction markers, E-cadherin, zonula occludens (ZO)-1 and Occludin, were decreased after PM2.5 exposure in vivo and in vitro by using RT-qPCR and immunofluorescence, with the increased expression of FADD. Moreover, down-regulation of FADD attenuated PM2.5-induced apoptosis and tight junction disruption in human airway epithelial cells.
conclusionTaken together, we demonstrated that PM2.5 aggravated epithelial tight junction disruption through apoptosis mediated by up-regulation of FADD in OVA-induced model.
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