ArticleJournal of thoracic disease2017
Urban particulate matter triggers lung inflammation via the ROS-MAPK-NF-κB signaling pathway.
Article in Journal of thoracic disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 1 of them a synthesis that pooled it.
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Who cites it
129 citing papers in PubMed, 1 synthesis or guideline pooled it, 263 citations in OpenAlex.
- Toxicological Effects of Air Pollutants on Human Airway Cell Models Using Air-liquid Interface Systems: A Systematic Review.Current environmental health reports · 2025Pooled it
- Association between polyphenols and inhalation-induced oxidative stress in chronic lung diseases: A systematic review.Biomedical reports · 2026Article
- In vitro approaches to assess respiratory toxicity from volatile organic compounds: an in-depth review.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Article
- Senolytics Reverse PMCardiovascular toxicology · 2026Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Nano-Encapsulated Black Bean-CultivatedNutrients · 2026Article
- Airborne Particulate Matter as an Emerging Driver of Gastric Carcinogenesis: Molecular Pathways Linking Inflammation and Cancer.International journal of molecular sciences · 2026Review
- Prediction of primary human targets and toxicity mechanisms of imidacloprid using integrativeToxicology reports · 2026Article
- RNAseq analysis demonstrates polarization state-dependent responses to ambient particulate matter in a particle composition-specific manner.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Associations between Environmental Persistent Free Radicals, Reactive Oxygen Species, and Oxidative Potential in Atmospheric Aerosols.ACS omega · 2026Article
- Copper-based nanozymes synergistically enhance Cuproptosis for psoriasis treatment.Materials today. Bio · 2026Article
- Immune, inflammatory, and metal biomarker profiles in chronic respiratory diseases receiving oligo-fucoidan under ambient PM₂.₅ exposure.Scientific reports · 2026Article
- Prognostic impact of PMiScience · 2026Article
- Genetically predicted susceptibility to dust-induced lung diseases and risk of autoimmune diseases: a two sample Mendelian randomization study.Journal of neuroinflammation · 2026Article
- Differential Circulating miRNA Responses to PM Exposure in Healthy and Diabetes Mellitus Patients: Implications for Lung Cancer Susceptibility.International journal of molecular sciences · 2026Article
- Changes in Serum Proteins in Firefighters Responding to the 2025 Los Angeles Urban Conflagrations.Journal of occupational and environmental medicine · 2026Article
- The Application and Challenges of Stem Cell-Derived Extracellular Vesicles in Inhalation Lung Injury.International journal of nanomedicine · 2026Review
- Qingre-Huatan-Liqi formula attenuates FPM-induced lung injury via modulation of MAPK signaling and NETs formation.Frontiers in pharmacology · 2026Article
- Flavonoids: Potential New Drug Candidates for Attenuating Vascular Remodeling in Pulmonary Hypertension.International journal of molecular sciences · 2025Review
69 more citing papers are in PubMed but not listed here.
Corrections and comments
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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
backgroundParticulate matter (PM) is a high risk factor for various respiratory diseases and triggers an inflammatory response in lung tissues. However, the molecular mechanism of the PM-induced inflammatory response is incompletely understood.
methodsHuman bronchial epithelial cells (HBECs) were treated with the urban PM 1649b for assessment of the inflammatory response. The intracellular level of reactive oxygen species (ROS) was measured by flow cytometry. PM-activated signaling pathways were addressed with specific inhibitors.
resultsPM increased the expression of interleukin (IL)-1β, IL-6, IL-8, matrix metalloproteinase (MMP)-9 and cyclooxygenase (COX)-2 in a dose-dependent manner. ROS generation and activation of MAPK (ERK, JNK, p38 MAPK) and NF-κB pathways were detected in PM-exposed HBECs. Pretreatment with N-acetylcysteine (NAC) led to the inflammatory response, ROS level and activation of the MAPK and NF-κB pathways to be attenuated. Blockade of ERK, JNK or p38 MAPK pathway with specific inhibitor prevented the release of pro-inflammatory cytokines and activation of the NF-κB pathway. Inhibition of the NF-κB pathway reduced the expression of pro-inflammatory cytokines.
conclusionsPM exposure enhanced the airway inflammatory response significantly through ROS-mediated activation of MAPK (ERK, JNK, p38 MAPK) and downstream NF-κB signaling pathways. Oxidative stress appeared to be the key regulator for PM-induced lung inflammation. These results suggested the molecular mechanism of lung inflammation caused by PM.
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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.