ArticleThe Korean journal of internal medicine2020
N-acetylcysteine decreases airway inflammation and responsiveness in asthma by modulating claudin 18 expression.
Article in The Korean journal of internal medicine, 2020. 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, 33 citations in OpenAlex.
- Targeting Tight Junction Proteins to Restore Airway Epithelial Barrier Function in Asthma.Current allergy and asthma reports · 2026Review
- Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies.Seminars in immunopathology · 2026Review
- The ratio of circulatory levels of sphingolipids to steroids predicts asthma exacerbations.Nature communications · 2026Article
- Garlic-derived allyl sulfides attenuate house dust mite-induced allergic airway inflammation associated with reduced PI3K/NF-κB signaling.Frontiers in pharmacology · 2026Article
- Protective effect of micheliolide against inflammation and oxidative stress in asthma through the MAPK/NF-κB signalling pathway.The World Allergy Organization journal · 2025Article
- Antiviral effect of Bromelain combined with acetylcysteine against SARS-CoV-2 Omicron variant.Scientific reports · 2025Article
- Advances in the Use ofAntioxidants (Basel, Switzerland) · 2023Review
- Hypermethylation of RNF125 promotes autophagy-induced oxidative stress in asthma by increasing HMGB1 stability.iScience · 2023Article
- Airway remodeling heterogeneity in asthma and its relationship to disease outcomes.Frontiers in physiology · 2023Review
- A network-biology led computational drug repurposing strategy to prioritize therapeutic options for COVID-19.Heliyon · 2022Article
- Claudin-18 expression under hyperoxia in neonatal lungs of bronchopulmonary dysplasia model rats.Frontiers in pediatrics · 2022Article
- The Impact of Environmental Pollutants on Barrier Dysfunction in Respiratory Disease.Allergy, asthma & immunology research · 2021Review
- Effects of Air Pollutants on Airway Diseases.International journal of environmental research and public health · 2021Review
- [A review on the effect of Claudin-18 on bronchopulmonary dysplasia in preterm infants].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021Review
- The Degradation of Airway Epithelial Tight Junctions in Asthma Under High Airway Pressure Is Probably Mediated by Piezo-1.Frontiers in physiology · 2021Article
- COVID-19: The Potential Role of Copper and N-acetylcysteine (NAC) in a Combination of Candidate Antiviral Treatments Against SARS-CoV-2.In vivo (Athens, Greece) · 2020Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsN-acetylcysteine (NAC) affects signaling pathways involved in apoptosis, angiogenesis, cell growth and arrest, redox-regulated gene expression, and the inflammatory response. However, it is not known how the signal mechanism for tight junctional protein claudin (CLDN) 18 is regulated in asthma patients.
methodsTo investigate the effects of NAC on CLDN18 expression in a mouse model of asthma, and to assess plasma levels of CLDN18 in asthma patients. A murine model of asthma induced by ovalbumin (OVA) was established using wild-type BALB/c female mice, and the levels of CLDNs, phosphorylated-pyruvate dehydrogenase kinase 1 (p-PDK1), and protein kinase B (Akt) pathway proteins following NAC treatment were examined by Western blotting and immunohistochemistry. In addition, the plasma levels of CLDN18 were evaluated in asthmatic patients and control subjects.
resultsNAC diminished OVA-induced airway hyper-responsiveness and inflammation. Levels of CLDN18 protein were higher in lung tissue from OVA mice than tissue from control mice, and were increased by treatment with NAC or dexamethasone. Treatment with NAC or dexamethasone decreased the OVA-induced increase in interleukin-1α protein levels. Although treatment with NAC increased OVA-induced p-PDK1 protein levels, it decreased phosphorylated Akt (pAkt)/Akt levels. Soluble CLDN18 levels were lower in patients with asthma than in controls and were correlated with the percentage of neutrophils, forced expiratory volume in 1 second (FEV1)/forced vital capacity % (FVC%) and FEV1%.
conclusionCLDN18 plays a role in the pathogenesis of asthma and NAC diminishes airway inflammation and responsiveness by modulating CLDN18 expression.
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