ArticleJournal of cellular and molecular medicine2020
IL-17A-producing T cells exacerbate fine particulate matter-induced lung inflammation and fibrosis by inhibiting PI3K/Akt/mTOR-mediated autophagy.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 109 citations in OpenAlex.
- Clinical investigation on nebulized human umbilical cord MSC-derived extracellular vesicles for pulmonary fibrosis treatment.Signal transduction and targeted therapy · 2025Trial
- Dust Fall Microplastics from a Megacity of China Inhibit Autophagy via the PI3K/Akt/mTOR Pathway.Environment & health (Washington, D.C.) · 2025Article
- IL-17A regulates airway remodelling in COPD through the PI3K/AKT/mTOR pathway.Scientific reports · 2025Article
- Chitosan Nanoparticle-EncapsulatedInternational journal of molecular sciences · 2025Article
- Cromolyn sodium reduces LPS-induced pulmonary fibrosis by inhibiting the EMT process enhanced by MC-derived IL-13.Respiratory research · 2025Article
- The Adverse Health Effects of Air Pollution from Sugarcane Burning: A Scoping Review of Observational and Experimental Evidence.Environmental health perspectives · 2025Article
- Preclinical research of dihydromyricetin for fibrotic diseases.Frontiers in pharmacology · 2025Review
- MAP3K19 Promotes the Progression of Tuberculosis-Induced Pulmonary Fibrosis Through Activation of the TGF-β/Smad2 Signaling Pathway.Molecular biotechnology · 2024Article
- Autophagy in Disease Onset and Progression.Aging and disease · 2024Review
- Effect of air pollution on asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2024Review
- Environmental pollutants and phosphoinositide signaling in autoimmunity.Journal of hazardous materials · 2024Review
- Nintedanib Mitigates Radiation-Induced Pulmonary Fibrosis by Suppressing Epithelial Cell Inflammatory Response and Inhibiting Fibroblast-to-Myofibroblast Transition.International journal of biological sciences · 2024Article
- Pregnane X receptor reduces particulate matter-induced type 17 inflammation in atopic dermatitis.Frontiers in immunology · 2024Article
- PM2.5 Promotes Macrophage-Mediated Inflammatory Response Through Airway Epithelial Cell-Derived Exosomal miR-155-5p.Journal of inflammation research · 2024Article
- Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model.Burns & trauma · 2024Article
- Combination of androgen and estrogen improves asthma by mediating Runx3 expression.International journal of medical sciences · 2024Article
- Luminol-conjugated cyclodextrin biological nanoparticles for the treatment of severe burn-induced intestinal barrier disruption.Burns & trauma · 2024Article
- Insights into innate immune cell evasion byFrontiers in immunology · 2024Review
- Grape Seed Proanthocyanidin Ameliorates LPS-induced Acute Lung Injury By Modulating M2a Macrophage Polarization Via the TREM2/PI3K/Akt Pathway.Inflammation · 2023Article
- LncRNA TUG1 promotes pulmonary fibrosis progression via up-regulating CDC27 and activating PI3K/Akt/mTOR pathway.Epigenetics · 2023Article
Corrections and comments
- Retracted
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fine particulate matter (PM2.5) is the primary air pollutant that is able to induce airway injury. Compelling evidence has shown the involvement of IL-17A in lung injury, while its contribution to PM2.5-induced lung injury remains largely unknown. Here, we probed into the possible role of IL-17A in mouse models of PM2.5-induced lung injury. Mice were instilled with PM2.5 to construct a lung injury model. Flow cytometry was carried out to isolate γδT and Th17 cells. ELISA was adopted to detect the expression of inflammatory factors in the supernatant of lavage fluid. Primary bronchial epithelial cells (mBECs) were extracted, and the expression of TGF signalling pathway-, autophagy- and PI3K/Akt/mTOR signalling pathway-related proteins in mBECs was detected by immunofluorescence assay and Western blot analysis. The mitochondrial function was also evaluated. PM2.5 aggravated the inflammatory response through enhancing the secretion of IL-17A by γδT/Th17 cells. Meanwhile, PM2.5 activated the TGF signalling pathway and induced EMT progression in bronchial epithelial cells, thereby contributing to pulmonary fibrosis. Besides, PM2.5 suppressed autophagy of bronchial epithelial cells by up-regulating IL-17A, which in turn activated the PI3K/Akt/mTOR signalling pathway. Furthermore, IL-17A impaired the energy metabolism of airway epithelial cells in the PM2.5-induced models. This study suggested that PM2.5 could inhibit autophagy of bronchial epithelial cells and promote pulmonary inflammation and fibrosis by inducing the secretion of IL-17A in γδT and Th17 cells and regulating the PI3K/Akt/mTOR signalling pathway.
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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.