There is now considerable evidence suggesting a role for platelets as inflammatory cells. These actions are distinct from their classically known actions performed during thrombosis and haemostasis; and include the expression of adhesion molecules and contact dependent activation of leukocytes, the release of a plethora of inflammatory mediators, activation of cells of the adaptive immune response, and the ability to migrate and undergo chemotaxis. Chronic asthma is a disease characterised by a mixed inflammatory cell pulmonary infiltrate, airways hyper-responsiveness, and tissue remodelling. Clinical data from asthmatic patients reveals changes in platelet behaviour and function during or after allergen exposure (1). Furthermore, mouse models of allergic inflammation demonstrate a role for intact platelets in eosinophil and lymphocyte recruitment to the lungs, a mechanism that is platelet P-selectin dependent (2). Models of chronic inflammation reveal a participation in platelets in tissue remodelling events whereby platelet depletion was found to be more effective in suppressing airway remodelling processes then the administration of a glucocorticosteroid (3). This process of destruction and repair to the architecture of airway tissue is therefore perhaps enhanced by platelet activation and recent evidence demonstrates platelets can undergo chemotaxis towards allergen via an IgE dependent process and migrate through inflamed tissue, where they localise to specific tissue sites. Indeed, platelets have also been shown to localise to, and interact with airway dendritic cells, suggestive of a link between the innate and adaptive immune response. Thus, these actions may lead to alterations in lung function as platelet depletion suppresses airways hyper-responsiveness in allergic rabbits (4). Thus, further investigations into the role of platelets in inflammation may be beneficial in the search for future therapeutic targets in the treatment of asthma.