Protection from experimental asthma by an endogenous bronchodilator.
Journal Article (Journal Article)
Mechanisms that protect against asthma remain poorly understood. S-nitrosoglutathione (GSNO), an endogenous bronchodilator, is depleted from asthmatic airways, suggesting a protective role. We report that, following allergen challenge, wild-type mice exhibiting airway hyperresponsivity have increased airway levels of the enzyme GSNO reductase (GSNOR) and are depleted of lung S-nitrosothiols (SNOs). In contrast, mice with genetic deletion of GSNOR exhibit increases in lung SNOs and are protected from airway hyperresponsivity. Our results indicate that endogenous SNOs, governed by GSNOR, are critical regulators of airway responsivity and may provide new therapeutic approaches to asthma.
Full Text
Duke Authors
Cited Authors
- Que, LG; Liu, L; Yan, Y; Whitehead, GS; Gavett, SH; Schwartz, DA; Stamler, JS
Published Date
- June 10, 2005
Published In
Volume / Issue
- 308 / 5728
Start / End Page
- 1618 - 1621
PubMed ID
- 15919956
Pubmed Central ID
- PMC2128762
Electronic International Standard Serial Number (EISSN)
- 1095-9203
Digital Object Identifier (DOI)
- 10.1126/science.1108228
Language
- eng
Conference Location
- United States