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Published on: March 30, 2017
Protection from experimental asthma by an endogenous bronchodilator
Loretta G Que1, Limin Liu, Yun Yan
1Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Science (New York, N.Y.)
|May 28, 2005
Summary
Endogenous S-nitrosothiols (SNOs), regulated by GSNO reductase (GSNOR), protect against asthma. Inhibiting GSNOR increases protective SNOs and reduces airway hyperresponsivity, offering potential new asthma therapies.
Area of Science:
- Immunology
- Pulmonology
- Biochemistry
Background:
- Asthma pathogenesis involves poorly understood protective mechanisms.
- S-nitrosoglutathione (GSNO), an endogenous bronchodilator, is decreased in asthmatic airways, implying a protective role.
- Airway hyperresponsivity is a key feature of asthma.
Purpose of the Study:
- To investigate the role of endogenous S-nitrosothiols (SNOs) in airway hyperresponsivity.
- To determine the involvement of GSNO reductase (GSNOR) in regulating SNO levels and asthma.
- To explore potential therapeutic strategies for asthma based on SNO regulation.
Main Methods:
- Allergen challenge in wild-type and GSNOR-deficient mice.
- Measurement of airway hyperresponsivity.
- Quantification of lung S-nitrosothiols (SNOs) and GSNO reductase (GSNOR) levels.
Main Results:
- Wild-type mice challenged with allergen showed increased GSNOR, decreased lung SNOs, and developed airway hyperresponsivity.
- Mice genetically deficient in GSNOR exhibited elevated lung SNOs.
- GSNOR-deficient mice were protected from allergen-induced airway hyperresponsivity.
Conclusions:
- Endogenous SNOs, modulated by GSNOR, are crucial regulators of airway responsivity.
- GSNOR activity is linked to airway hyperresponsivity in asthma.
- Targeting GSNOR to modulate SNO levels represents a potential therapeutic avenue for asthma.
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