The role of adenosine as a novel bronchoprovocant in asthma.

Abstract

There is evidence that bronchial hyperresponsiveness to inhaled adenosine may be a better marker of airway allergic inflammation than bronchial hyperresponsiveness to other spasmogens. Here the authors review the most recent development in this area of rapidly evolving clinical research, focusing on the putative role of adenosine as a useful bronchoprovocant in asthma. New studies have provided evidence that hyperresponsiveness to AMP strongly correlates with sputum, blood/bronchial tissue eosinophilia and exhaled nitric oxide, whereas hyperresponsiveness to methacholine is related to changes in forced expiratory volume in 1 s, thus reflecting changes in airway caliber and functional state. Other recent studies have emphasized that the state of atopy is critically important in the bronchial response to inhaled AMP. The early finding that in people with asthma treatment with inhaled glucocorticosteroids significantly reduces airway responsiveness to AMP, as compared with other spasmogens such as methacholine or bradykinin, has been confirmed by recent reports which have also outlined that this is an early phenomenon. Taken together these studies evidence that hyperresponsiveness to inhaled adenosine may be a better marker of airway allergic inflammation than hyperresponsiveness to other spasmogens. This peculiar property of adenosine suggests that bronchial provocation with inhaled adenosine could provide a reliable noninvasive tool for monitoring asthma activity/progression, and assessing the response to antiinflammatory treatments.