Format

Send to

Choose Destination
Science. 2005 Jun 10;308(5728):1618-21. Epub 2005 May 26.

Protection from experimental asthma by an endogenous bronchodilator.

Author information

1
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.

Abstract

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.

PMID:
15919956
PMCID:
PMC2128762
DOI:
10.1126/science.1108228
[Indexed for MEDLINE]
Free PMC Article

Publication types, MeSH terms, Substances, Grant support

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center