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Protection from experimental asthma by an endogenous bronchodilator.

Science (New York, N.Y.) (2005-05-28)
Loretta G Que, Limin Liu, Yun Yan, Gregory S Whitehead, Stephen H Gavett, David A Schwartz, Jonathan S Stamler
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.

MATERIALS
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Brand
Product Description

Sigma-Aldrich
Glutathione Reductase from baker's yeast (S. cerevisiae), ammonium sulfate suspension, 100-300 units/mg protein (biuret)