Source: Annual Congress 2002 - Cellular reactions in allergy in humans and animals
Disease area: Airway diseases

Abstract

Asthma is a chronic airway disease characterized by infiltration of inflammatory cells, epithelial cell damage and airway hyperresponsiveness (AHR). Nitric oxide, which is both a signaling and inflammatory molecule, plays an important role in asthma. NO, produced by constitutive NO synthase (NOS) present in the epithelial layer (eNOS), dilates airway smooth muscle and controls airway responsiveness. Whether NO, produced by eNOS, also modulates inflammatory cells and mediators in asthma is unknown. In this study, we investigated the effects of eNOS overexpression on asthmatic features in an animal model for allergic asthma. Therefore, control and eNOS overexpressing mice were sensitized and challenged with ovalbumin. One day after the last challenge, airway responsiveness to methacholine, cell numbers in the bronchoalveolar lavage (BAL) fluid, IgE levels in serum, and cytokine production by thoracic lymph nodes (TLN) were measured. AHR to methacholine was completely abolished in eNOS overexpressing ovalbumin challenged mice compared to control mice. Furthermore, eNOS overexpression reduced the increase in the number of lymphocytes and eosinophils in the BAL fluid of ovalbumin challenged mice by 50%. No difference in IgE production could be observed between control and eNOS overexpressing ovalbumin challenged mice, whereas eNOS overexpression inhibited IL-5 and IL-10 production by TLN compared with control mice. We conclude that eNOS overexpression results in attenuation of both ovalbumin-induced AHR and airway inflammation. Therefore, NO derived from eNOS might play a crucial role in the pathophysiology of asthma.

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R. Ten Broeke, G. Folkerts, R. De Crom, R. Van Haperen, V. Verwey, T. Leusink-Muis, I. Van Ark, F. De Clerck, F. Nijkamp (Utrecht, Rotterdam, The Netherlands). Overexpression of eNOS suppresses asthmatic features in a mouse model of allergic asthma. Eur Respir J 2002; 20: Suppl. 38, 300

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