ArticleRespiratory research2023
Azithromycin ameliorated cigarette smoke-induced airway epithelial barrier dysfunction by activating Nrf2/GCL/GSH signaling pathway.
Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 9 citations in OpenAlex.
- Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Research on the Mechanism of Natural Products Acting on Chronic Obstructive Pulmonary Disease.Food science & nutrition · 2026Review
- Pseudoephedrine Improves Chronic Obstructive Pulmonary Disease by Regulating Airway Senescence and Mitochondrial Function through PI3K/AKT/mTOR Axis.Biomolecules & therapeutics · 2026Article
- Metabolic Symbiosis Between Cancer Cells and Endothelial Cells: A Key Driver of Tumor Angiogenesis.Advances in experimental medicine and biology · 2026Review
- Nonpolysaccharide fraction ofFrontiers in pharmacology · 2026Article
- Mechanisms, Efficacy, Safety, and Pharmacoeconomics of Low-Dose, Long-Term Macrolide Antibiotics in the Treatment of Chronic Obstructive Pulmonary Disease: A Review.International journal of chronic obstructive pulmonary disease · 2026Review
- Involvement of mitochondrial unfolded protein response and activating transcription factor 4 in the mitochondrial damage pathway of BEAS-2B cells induced by cigarette smoke extracts.Journal of thoracic disease · 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
- [Research progress in the regulation of allergic rhinitis pathogenesis by the NRF2 pathway].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Review
- Article
- Effects of azithromycin on lung oxidative injury and immune function in mice infected withCentral-European journal of immunology · 2025Article
- Integrating bioinformatics and molecular experiments to reveal the critical role of the cellular energy metabolism-related marker PLA2G1B in COPD epithelial cells.Frontiers in immunology · 2025Article
- Transcriptional analysis of primary ciliary dyskinesia airway cells reveals a dedicated cilia glutathione pathway.JCI insight · 2024Article
- Bone Formation and Maintenance in Oral Surgery: The Decisive Role of the Immune System-A Narrative Review of Mechanisms and Solutions.Bioengineering (Basel, Switzerland) · 2024Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAirway epithelium is the first barrier against environmental insults, and epithelial barrier dysfunction caused by cigarette smoke (CS) is particularly relevant to chronic obstructive pulmonary disease (COPD) progression. Our study was to determine whether Azithromycin (AZI) ameliorates CS-induced airway epithelial barrier dysfunction and the underlying mechanisms.
methodsPrimary bronchial epithelial cells (PBECs), human bronchial epithelial cells (HBECs), Sprague Dawley rats and nuclear factor erythroid 2-related factor 2 (Nrf2)-/- mice were pretreated with AZI and subsequently exposed to CS. Transepithelial electronic resistance (TEER), junction proteins as well as pro-inflammatory cytokines and apoptosis markers were examined to assess epithelial barrier dysfunction. Metabolomics study was applied to explore the underlying mechanism of AZI.
resultsCS-induced TEER decline and intercellular junction destruction, accompanied with inflammatory response and cell apoptosis in PBECs were restored by AZI dose-dependently, which were also observed in CS-exposed rats. Mechanistically, GSH metabolism pathway was identified as the top differentially impacted pathway and AZI treatment upregulated the activities of glutamate cysteine ligase (GCL) and the contents of metabolites in GSH metabolic pathway. Furthermore, AZI apparently reversed CS-induced Nrf2 suppression, and similar effects on airway epithelial barrier dysfunction were also found for Nrf2 agonist tert-butylhydroquinone and vitamin C. Finally, deletion of Nrf2 in both HBECs and C57BL/6N mice aggravated CS-induced GSH metabolism imbalance to disrupt airway epithelial barrier and partially deprived the effects of AZI.
conclusionThese findings suggest that the clinical benefits of AZI for COPD management are related with the protection of CS-induced airway epithelial barrier dysfunction via activating Nrf2/GCL/GSH pathway, providing potential therapeutic strategies for COPD.
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