Cysteinyl leukotrienes (cysLTs) are bronchoconstricting lipid mediators that amplify eosinophilic airway inflammation by incompletely understood mechanisms. We recently found that LTC 4, the parent cysLT, potently activates platelets in vitro and induces airway eosinophilia in allergen-sensitized and-challenged mice by a platelet-and type 2 cysLT receptor–dependent pathway. We now demonstrate that this pathway requires production of thromboxane A 2 and signaling through both hematopoietic and lung tissue–associated T prostanoid (TP) receptors. Intranasal administration of LTC 4 to OVA-sensitized C57BL/6 mice markedly increased the numbers of eosinophils in the bronchoalveolar lavage fluid, while simultaneously decreasing the percentages of eosinophils in the blood by a TP receptor–dependent mechanism. LTC 4 upregulated the expressions of ICAM-1 and VCAM-1 in an aspirin-sensitive and TP receptor–dependent manner. Both hematopoietic and nonhematopoietic TP receptors were essential for LTC 4 to induce eosinophil recruitment. Thus, the autocrine and paracrine functions of thromboxane A 2 act downstream of LTC 4/type 2 cysLT receptor signaling on platelets to markedly amplify eosinophil recruitment through pulmonary vascular adhesion pathways. The findings suggest applications for TP receptor antagonists in cases of asthma with high levels of cysLT production.