ArticleRespiratory research2006
Overexpression of endothelial nitric oxide synthase suppresses features of allergic asthma in mice.
Article in Respiratory research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 72 citations in OpenAlex.
- Use of continuous positive airway pressure reduces airway reactivity in adults with asthma.The European respiratory journal · 2013Trial
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- Role of Nitric Oxide Synthases in Respiratory Health and Disease: Insights from Triple Nitric Oxide Synthases Knockout Mice.International journal of molecular sciences · 2024Review
- Nitric Oxide: The Missing Factor in COVID-19 Severity?Medical sciences (Basel, Switzerland) · 2021Article
- Review - Nutraceuticals Can Target Asthmatic Bronchoconstriction: NADPH Oxidase-Dependent Oxidative Stress, RhoA and Calcium Dynamics.Journal of asthma and allergy · 2021Review
- Glucagon-like peptide 1: A potential anti-inflammatory pathway in obesity-related asthma.Pharmacology & therapeutics · 2017Review
- Epigenetic regulation of nitric oxide synthase 2, inducible (Nos2) by NLRC4 inflammasomes involves PARP1 cleavage.Scientific reports · 2017Article
- Anti-interleukin-33 Reduces Ovalbumin-Induced Nephrotoxicity and Expression of Kidney Injury Molecule-1.International neurourology journal · 2016Article
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- Statins in Asthma: Potential Beneficial Effects and Limitations.Pulmonary medicine · 2015Review
- Novel therapeutic strategies for adult obese asthmatics.Immunology and allergy clinics of North America · 2014Review
- Measurement of airway function using invasive and non-invasive methods in mild and severe models for allergic airway inflammation in mice.Frontiers in pharmacology · 2014Article
- Article
- Mitochondrial dysfunction in metabolic syndrome and asthma.Journal of allergy · 2013Article
- Particulate matter, DNA methylation in nitric oxide synthase, and childhood respiratory disease.Environmental health perspectives · 2012Article
- Competitive metabolism of L-arginine: arginase as a therapeutic target in asthma.Journal of biomedical research · 2011Article
- D-4F, an apoA-1 mimetic, decreases airway hyperresponsiveness, inflammation, and oxidative stress in a murine model of asthma.Journal of lipid research · 2011Article
- Nitric oxide in asthma physiopathology.ISRN allergy · 2011Article
- Asymmetric dimethylarginine potentiates lung inflammation in a mouse model of allergic asthma.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- Nitric oxide synthase enzymes in the airways of mice exposed to ovalbumin: NOS2 expression is NOS3 dependent.Mediators of inflammation · 2010Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAsthma is associated with airway hyperresponsiveness and enhanced T-cell number/activity on one hand and increased levels of exhaled nitric oxide (NO) with expression of inducible NO synthase (iNOS) on the other hand. These findings are in paradox, as NO also relaxes airway smooth muscle and has immunosuppressive properties. The exact role of the endothelial NOS (eNOS) isoform in asthma is still unknown. We hypothezised that a delicate regulation in the production of NO and its bioactive forms by eNOS might be the key to the pathogenesis of asthma.
methodsThe contribution of eNOS on the development of asthmatic features was examined. We used transgenic mice that overexpress eNOS and measured characteristic features of allergic asthma after sensitisation and challenge of these mice with the allergen ovalbumin.
resultseNOS overexpression resulted in both increased eNOS activity and NO production in the lungs. Isolated thoracic lymph nodes cells from eNOS overexpressing mice that have been sensitized and challenged with ovalbumin produced significantly less of the cytokines IFN-gamma, IL-5 and IL-10. No difference in serum IgE levels could be found. Further, there was a 50% reduction in the number of lymphocytes and eosinophils in the lung lavage fluid of these animals. Finally, airway hyperresponsiveness to methacholine was abolished in eNOS overexpressing mice.
conclusionThese findings demonstrate that eNOS overexpression attenuates both airway inflammation and airway hyperresponsiveness in a model of allergic asthma. We suggest that a delicate balance in the production of bioactive forms of NO derived from eNOS might be essential in the pathophysiology of asthma.
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