Adenosine levels in the exhaled breath condensate: a potential surrogate marker of airway inflammation.

We would like to congratulate HUSZAR et al. [1] on their important and meticulous study demonstrating elevated adenosine levels in the exhaled breath condensate of atopic asthmatic subjects compared to nonatopic controls. Their findings are in agreement with and somewhat complementary to previous data obtained from bronchoalveolar lavage fluid of patients with asthma and chronic obstructive pulmonary disease [2], thus adding to the notion that adenosine may have a pathogenic role in chronic inflammatory disorders of the airways [3]. Unfortunately, our knowledge on the role of adenosine in physiological and pathological conditions remains limited by the availability of potent and selective adenosinereceptor antagonists for use in humans. In relation to the findings of the present study, it is important to emphasise that these atopic asthmatics were all sensitised to grass pollen and all studied during the grass pollen season. Natural exposure to aeroallergens is likely to modulate the level of airway inflammation not only in asthma but also in hay fever patients. We have repeatedly shown that nonasthmatic individuals with allergic rhinitis also exhibit features of active inflammation in the lower airways which deteriorates during natural allergen exposure [4, 5]. It is therefore likely that the results of the study by HUSZAR et al. [1] could also be interpreted as a response to natural allergen exposure reflecting inflammatory changes occurring at airway levels. Indeed, the pioneering work by MANN et al. [6] clearly demonstrated a significant increase in the plasma levels of adenosine following allergen challenge in subjects with atopic asthma. Although the inclusion of an atopic control group would have enhanced the quality of the paper by HUSZAR et al. [6], an important implication of these findings is that adenosine levels in the exhaled breath condensate could be valuable in assessing disease activity in relation to airway inflammation. This will obviously require rigorous testing in future long-term studies where seasonal changes in exhaled breath condensate adenosine levels are clearly related to natural allergen exposure/avoidance.