How eNOS Overexpression Affects Allergic Asthma in Mice
Author Information
Author(s): Robert Ten Broeke, Rini De Crom, Rien Van Haperen, Vivienne Verweij, Thea Leusink-Muis, Ingrid Van Ark, Fred De Clerck, Frans P Nijkamp, Gert Folkerts
Primary Institution: Utrecht University
Hypothesis
A delicate regulation in the production of nitric oxide by endothelial nitric oxide synthase (eNOS) might be key to the pathogenesis of asthma.
Conclusion
eNOS overexpression reduces airway inflammation and hyperresponsiveness in a mouse model of allergic asthma.
Supporting Evidence
- eNOS overexpression resulted in increased eNOS activity and NO production in the lungs.
- eNOS overexpressing mice produced significantly less cytokines IFN-γ, IL-5, and IL-10 after allergen challenge.
- There was a 50% reduction in lymphocytes and eosinophils in the lung lavage fluid of eNOS overexpressing mice.
- Airway hyperresponsiveness to methacholine was abolished in eNOS overexpressing mice.
Takeaway
Scientists found that making a special protein called eNOS work more in mice helps them breathe better when they have asthma.
Methodology
Transgenic mice overexpressing eNOS were sensitized and challenged with ovalbumin, and various asthma-related features were measured.
Participant Demographics
Transgenic mice used in the study.
Statistical Information
P-Value
p<0.001
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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