The administration of clopidogrel attenuates airway hyperresponsiveness and airway inflammation in an ovalbumin specific allergic asthma model

Background and objective Cysteinyl leukotrienes (LTs) contribute to airway inflammation by interacting with type 1 and 2 cysteinyl leukotriene receptors as well as not clearly known type 3 leukotriene receptors. In contrast to LTC4 and LTD4, LTE4 is weak agonist at type 1 and 2 cysteinyl leukotriene receptors. Although LTE4 plays a key role in airway inflammation, our understanding of its potential receptor remains unclear. We investigated the effects of clopidogrel in the development of allergic airway inflammation using mouse asthma model and eosinophil cell-line.