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


  • eng

Conference Location

  • United States