ArticleEnvironmental pollution (Barking, Essex : 1987)2022
Diesel exhaust particles distort lung epithelial progenitors and their fibroblast niche.
Article in Environmental pollution (Barking, Essex : 1987), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 39 citations in OpenAlex.
- Lung organoids and organ-on-a-chip models in respiratory disease research: advances, applications, and challenges.Respiratory research · 2026Review
- The application progress of organoid technology in the toxicity assessment of environmental pollutants.Cell biology and toxicology · 2026Review
- Organoid for Air Pollution Toxicity Assessment: Advances and Environmental Applicability.Environment & health (Washington, D.C.) · 2025Review
- Recent Applications of Lung Organoid and Lung-on-a-Chip Technologies for Evaluating the Toxicity of Fine Particulate Matter.International journal of stem cells · 2025Review
- Air Pollutants in Puerto Rico: Key Pollutants and Carcinogenic Properties.International journal of environmental research and public health · 2025Review
- Particulate matter air pollution: effects on the respiratory system.The Journal of clinical investigation · 2025Review
- The Role and Phagocytic Mechanisms of Alveolar Macrophages in Inflammatory Responses Induced by Diesel Exhaust Particles.Environmental science & technology · 2025Article
- Towards a Better Understanding of the Human Health Risk of Per- and Polyfluoroalkyl Substances Using Organoid Models.Bioengineering (Basel, Switzerland) · 2025Article
- Fibroblast-derived osteoglycin promotes epithelial cell repair.NPJ Regenerative medicine · 2025Article
- Long-term exposure to diesel exhaust particles induces concordant changes in DNA methylation and transcriptome in human adenocarcinoma alveolar basal epithelial cells.Epigenetics & chromatin · 2024Article
- The stress-responsive cytotoxic effect of diesel exhaust particles on lymphatic endothelial cells.Scientific reports · 2024Article
- Toxicity of particles derived from combustion of Ethiopian traditional biomass fuels in human bronchial and macrophage-like cells.Archives of toxicology · 2024Article
- Impact of particulate air pollution on airway injury and epithelial plasticity; underlying mechanisms.Frontiers in immunology · 2024Review
- Cigarette smoke restricts the ability of mesenchymal cells to support lung epithelial organoid formation.Frontiers in cell and developmental biology · 2023Article
- Lung Organoids for Hazard Assessment of Nanomaterials.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by inflammation and impaired tissue regeneration, and is reported as the fourth leading cause of death worldwide by the Centers for Disease Control and Prevention (CDC). Environmental pollution and specifically motor vehicle emissions are known to play a role in the pathogenesis of COPD, but little is still known about the molecular mechanisms that are altered following diesel exhaust particles (DEP) exposure. Here we used lung organoids derived from co-culture of alveolar epithelial progenitors and fibroblasts to investigate the effect of DEP on the epithelial-mesenchymal signaling niche in the distal lung, which is essential for tissue repair. We found that DEP treatment impaired the number as well as the average diameter of both airway and alveolar type of lung organoids. Bulk RNA-sequencing of re-sorted epithelial cells and fibroblasts following organoid co-culture shows that the Nrf2 pathway, which regulates antioxidants' activity, was upregulated in both cell populations in response to DEP; and WNT/β-catenin signaling, which is essential to promote epithelial repair, was downregulated in DEP-exposed epithelial cells. We show that pharmacological treatment with anti-oxidant agents such as N-acetyl cysteine (NAC) or Mitoquinone mesylate (MitoQ) reversed the effect of DEP on organoids growth. Additionally, a WNT/β-catenin activator (CHIR99021) successfully restored WNT signaling and promoted organoid growth upon DEP exposure. We propose that targeting oxidative stress and specific signaling pathways affected by DEP in the distal lung may represent a strategy to restore tissue repair in COPD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.