Platelets in Asthma: Does Size Matter?

activation and an increased release of growth factors such as brain-derived neurotrophic factor (BDNF) [7–11] . On the other hand, platelets from patients with asthma have been postulated to be less responsive to various stimulants such as collagen, adenosine diphosphate (ADP) [12] , platelet-activating factor (PAF) [13] , and arachidonic acid [14] , suggesting that platelets might be ‘exhausted’ as a consequence of chronic activation [15] . Thus, the precise phenotype and role of platelets in patients with asthma are still incompletely understood. In this issue of Respiration, Sun et al. [16] investigate the mean platelet volume (MPV) of 85 patients with stable asthma and of 85 patients with exacerbated asthma and compare the results to those of a group of 85 healthy volunteers matched for age, gender, BMI, and smoking history. The authors show that patients with stable asthma display a significantly lower MPV (10.3 fl) compared to healthy controls (10.7 fl). In patients with an acute exacerbation of asthma, the MPV was even lower (9.8 fl) and correlated negatively with their serum levels of Creactive protein. These results add new evidence to the ongoing discussion on the role and phenotype of platelets in asthma. It might be speculated that ‘exhausted’ platelets are smaller in size due to chronic activation and chronic mediator release. However, the neurotrophin Platelets are anucleated cells which are small in size, simple in structure, and phylogenetically older than leukocytes. Therefore, these cells are often neglected and their function is thought to be limited to hemostasis. However, there is now a growing body of evidence that platelets play an essential role in various inflammatory diseases [1] . The overwhelming number and turnover of these cells in the human body (about 100 billion new platelets are released daily from bone marrow megakaryocytes), the unique ability of platelets to incorporate, store, and release mediators, and the multiple interactions of these cells with leukocytes and endothelial cells led to the concept that platelets are crucial players in the innate and adaptive immune responses of mammals [1] . It is therefore not surprising that there have been major efforts to elucidate the role of platelets in chronic inflammatory diseases such as asthma [2] . Data from animal models of asthma suggest that platelets infiltrate the airway wall after an allergen challenge, either by active migration [3] or by passive migration in platelet-leukocyte aggregates [4] , contributing to airway remodeling [5] and the development of airway hyperresponsiveness [6] . Clinical studies have shown a more complex picture of the platelet in asthma. On the one hand, platelets from patients with asthma are characterized by an increased Published online: May 28, 2014