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Friday, June 5, 2015

The role of platelets in allergic airway inflammation

Platelets are anucleated blood elements involved in hemostasis and thrombosis. It is now understood that they can also act as inflammatory cells and contribute to host defense against infection, performing many functions normally associated with leukocytes. Studies have shown that platelet depletion compromises ability to resist microorganism infection. Given that many inflammatory diseases are the result of inappropriate activation of defense pathways, it is likely inappropriate platelet activation contributes to the pathogenesis of these diseases. Idzko et al present the currently available data investigating the role of platelets in allergic airway inflammation and asthma (J Allergy Clin Immunol 2015; 135(6): 1416-23).

Of particular relevance to allergic inflammation, it has been shown that platelets express IgE receptors on their surfaces. They play an essential role in killing certain parasites, and platelet activation has been shown to accompany allergen exposure of sensitized patients. Platelet activation has also been observed in patients with asthma, measured as an increase in the levels of a number of platelet-derived mediators in peripheral blood or in bronchoalveolar lavage fluid (BAL). It is evident that platelets can release a number of spasmogens that can constrict human airway smooth muscle, including 5-HT, which has been demonstrated to induce bronchoconstriction in asthmatic patients. And platelet depletion has been reported to reduce allergen-induced bronchial hyperresponsiveness in sensitized rabbits, associated with a reduction in eosinophil infiltration in the lungs.


The increasing number of observations suggesting a dichotomy of platelet activation between the signaling involved in thrombosis and hemostasis and the activation during inflammatory responses has considerable implication. For example, using adenosine diphosphate (ADP), the authors have recently demonstrated that P2Y1 receptors are required for platelet activation by inflammatory stimuli, whereas PY12 receptors required for platelet aggregation have no such effect. The dichotomy of function opens the real possibility of developing anti-inflammatory and anti-allergic therapies that target the novel pathways of platelet activation. It also raises the possibility of finding novel biomarkers for assessing disease, given the clear role of platelets in leukocyte recruitment.

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