an immunoregulatory role of nitric oxide (NO) in the development of adaptive immune responses associated with allergic diseases is very important. The present study extended these observations by the examination of the reciprocal changes in characteristic immunologic parameters of the disease and NO level of bronchoalveolar lavage (Bal) cells under guinea pig model of acute asthma with multiple challenges. development of guinea pig Th2 mediated asthma was accompanied by increasing the level of allergic markers: ovalbumin (OVA) specific IgG and IL-4. We demonstrated that the infiltrate of airway cells contributes to NO synthesis in the respiratory tract during allergic inflammation. The level of intracellular NO formation significantly correlated with plasma allergen specific IgG value in OVA-induced asthma. The presented data evidence that the elevated intracellular NO level in BAL fluid may reflect a nitrosative stress in respiratory tract in general, when allergic asthma exacerbation is present.

The correlation between high exhaled nitric oxide levels and eosinophilic-mediated airway inflammation in patients with atopic asthma has been well documented. This generates prerequisites that a regulatory feedback mechanism exists between them. Therefore, the paper briefly describes evidence implementing biosynthesis, enzyme structural features, expression regulation of its isoforms and effects of nitric oxide, which have helped elucidate molecular mechanisms by which nitric oxide selectively promotes asthma exacerbation. In previous study we have demonstrated that airway infiltrate of immune cells contributes to NO synthesis in the respiratory tract during allergic inflammation under guinea pig model of acute asthma with multiple challenges. On the basis of these findings the authors posits that nitric oxide represents an additional signal of the induction of Th2 subset response and be considerably involved in the complex network of immune regulation distinctive for atopic asthma phenotype.