Effect of the Cysteinyl Leukotriene Antagonist Pranlukast on Transendothelial Migration of Eosinophils
Effect of the Cysteinyl Leukotriene Antagonist Pranlukast on Transendothelial Migration of Eosinophils
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DOI：
10.1159/000085424
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发表时间：
2005-06
影响因子：
2.8
通讯作者：
M. Nagata;Keiko Saito;I. Kikuchi;K. Hagiwara;M. Kanazawa
中科院分区：
文献类型：
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作者：
M. Nagata;Keiko Saito;I. Kikuchi;K. Hagiwara;M. Kanazawa
背景：有证据表明，白三烯受体拮抗剂（LTRA）可引起哮喘气道嗜酸性粒细胞的部分减少。虽然半胱氨酰白三烯（CysLTs）可以调节嗜酸性粒细胞炎症的发展，LTRA可能调节嗜酸性粒细胞对其他炎症分子参与过敏性炎症反应。孟鲁司特是一种LTRA，可抑制嗜酸性粒细胞对血小板活化因子（PAF）的跨内皮迁移（TEM）。本研究评估普仑司特（一种LTRA）是否改变嗜酸性粒细胞TEM对包括PAF和C-C趋化因子在内的化学引诱物的反应。方法：从健康个体的血液中分离的嗜酸性粒细胞与或不与普仑司特一起孵育。然后，我们评估了嗜酸性粒细胞穿越人脐静脉内皮细胞对LTD 4，嗜酸性粒细胞活化趋化因子，RANTES和PAF的反应。结果：普仑司特未改变嗜酸性粒细胞的自发迁移（n = 5）。据报告，0.1 µM LTD 4显著增强嗜酸性粒细胞TEM，1 µM普仑司特可阻断这种增强作用（p 0.1; n = 5）。结论：普仑司特钠对嗜酸性粒细胞迁移的抑制作用是高度特异性的，其机制可能与CysLT 1依赖性通路有关。
Background:Evidence shows that leukotriene receptor antagonist (LTRA) can cause a partial reduction of eosinophils in the asthmatic airway. Although cysteinyl leukotrienes (CysLTs) can regulate the development of eosinophilic inflammation, LTRA might modulate the eosinophilic response to other inflammatory molecules involved in allergic inflammation. Montelukast is an LTRA that inhibits eosinophil transendothelial migration (TEM) in response to platelet-activating factor (PAF). The present study evaluates whether pranlukast (an LTRA) modifies eosinophil TEM in response to chemoattractants including PAF and C-C chemokines. Methods: Eosinophils isolated from the blood of healthy individuals were incubated with or without pranlukast. We then evaluated eosinophil transmigration across human umbilical vein endothelial cells in response to LTD4, eotaxin, RANTES and PAF. Results: Pranlukast did not modify the spontaneous transmigration of eosinophils (n = 5). As reported, eosinophil TEM was significantly augmented by 0.1 µM LTD4 and this enhancement was blocked by 1 µM pranlukast (p 0.1; n = 5). Conclusion: The inhibitory effect of pranlukast on eosinophil transmigration is highly specific for the CysLT1-dependent pathway.