ArticleRespiratory research2009
Nitric oxide gas phase release in human small airway epithelial cells.
Article in Respiratory research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 55 citations in OpenAlex.
- Defining VOC signatures of airway epithelial cells with PM2.5 exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
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- Relationship between Particulate Matter (PMCanadian respiratory journal · 2020Article
- Ribosomal protein S3 gene silencing protects against experimental allergic asthma.British journal of pharmacology · 2017Article
- Migration of breast cancer cell lines in response to pulmonary laminin 332.Cancer medicine · 2017Article
- Extracellular ATP is involved in dsRNA-induced MUC5AC production via P2Y2R in human airway epithelium.Respiratory research · 2016Article
- The Role of the T lymphocytes and Remodeling in Asthma.Inflammation · 2016Article
- Modeling of the Nitric Oxide Transport in the Human Lungs.Frontiers in physiology · 2016Article
- Which biomarkers are effective for identifying Th2-driven inflammation in asthma?Current allergy and asthma reports · 2013Review
- Personalised medicine and asthma diagnostics/management.Current allergy and asthma reports · 2013Review
- Nitric oxide and superoxide mediate diesel particle effects in cytokine-treated mice and murine lung epithelial cells--implications for susceptibility to traffic-related air pollution.Particle and fibre toxicology · 2012Article
- Caveolin-1 knockout mice exhibit airway hyperreactivity.American journal of physiology. Lung cellular and molecular physiology · 2012Article
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- Phosphatidylinositol 3-kinase inhibitor suppresses inducible nitric oxide synthase expression in bronchiole epithelial cells in asthmatic rats.Molecular and cellular biochemistry · 2012Article
- Estrogen increases nitric-oxide production in human bronchial epithelium.The Journal of pharmacology and experimental therapeutics · 2011Article
- Modeling gas phase nitric oxide release in lung epithelial cells.Nitric oxide : biology and chemistry · 2011Article
- TGF-β2 reduces nitric oxide synthase mRNA through a ROCK-dependent pathway in airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Effects of atopy and rhinitis on exhaled nitric oxide values - a systematic review.Clinical and translational allergy · 2011Article
- Clinical update on the use of biomarkers of airway inflammation in the management of asthma.Journal of asthma and allergy · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAsthma is a chronic airway inflammatory disease characterized by an imbalance in both Th1 and Th2 cytokines. Exhaled nitric oxide (NO) is elevated in asthma, and is a potentially useful non-invasive marker of airway inflammation. However, the origin and underlying mechanisms of intersubject variability of exhaled NO are not yet fully understood. We have previously described NO gas phase release from normal human bronchial epithelial cells (NHBEs, tracheal origin). However, smaller airways are the major site of morbidity in asthma. We hypothesized that IL-13 or cytomix (IL-1beta, TNF-alpha, and IFN-gamma) stimulation of differentiated small airway epithelial cells (SAECs, generation 10-12) and A549 cells (model cell line of alveolar type II cells) in culture would enhance NO gas phase release.
methodsConfluent monolayers of SAECs and A549 cells were cultured in Transwell plates and SAECs were allowed to differentiate into ciliated and mucus producing cells at an air-liquid interface. The cells were then stimulated with IL-13 (10 ng/mL) or cytomix (10 ng/mL for each cytokine). Gas phase NO release in the headspace air over the cells was measured for 48 hours using a chemiluminescence analyzer.
resultsIn contrast to our previous result in NHBE, baseline NO release from SAECs and A549 is negligible. However, NO release is significantly increased by cytomix (0.51 +/- 0.18 and 0.29 +/- 0.20 pl.s-1.cm-2, respectively) reaching a peak at approximately 10 hours. iNOS protein expression increases in a consistent pattern both temporally and in magnitude. In contrast, IL-13 only modestly increases NO release in SAECs reaching a peak (0.06 +/- 0.03 pl.s-1.cm-2) more slowly (30 to 48 hours), and does not alter NO release in A549 cells.
conclusionWe conclude that the airway epithelium is a probable source of NO in the exhaled breath, and intersubject variability may be due, in part, to variability in the type (Th1 vs Th2) and location (large vs small airway) of inflammation.
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