@entity12824 and 1400 W prevents airway hyperresponsiveness during allergic reactions in XXXX .

@entity32 @entity10328 @entity1568 @entity6837 @entity12824 @entity19 @entity1110 @entity842 @entity224
1. The contribution of reactive @entity1568 species to the development of airway hyperresponsiveness in a @entity19 model of @entity32 was investigated by the use of selective inhibitors of @entity842 and @entity224 formation. 2. Sensitized @entity19 , repeatedly challenged with @entity10328 showed a significant (P<0.001, n=9) increase in airway responsiveness measured using whole body plethysmography. This hyperresponsiveness was accompanied by an influx of eosinophils into the airway lumen and increased levels of @entity10328 -specific serum IgE. 3. Treatment of @entity19 with the iNOS inhibitor 1400 W or the @entity1110 -oxidase inhibitor @entity12824 did not significantly alter cellular influx into the airway lumen nor serum @entity10328 specific IgE. In contrast, @entity12824 as well as 1400 W inhibited @entity10328 -induced airway hyperresponsiveness (P<0.001 and P<0.05 respectively, n=9). Furthermore, the airways of allergen challenged animals showed clear @entity6837 staining, which was mainly located in eosinophils. Remarkably, treatment with @entity12824 or 1400 W did not alter @entity6837 staining. 4. These data suggest that the development of airway hyperresponsiveness during the airway inflammation upon @entity10328 challenge is dependent on the release of both @entity224 and @entity842 and is therefore likely to be dependent on reactive @entity1568 species. This mechanism, however, is not reflected by @entity6837 formation in the airways.
