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首页> 外文期刊>Clinical and experimental allergy : >Interaction of suplatast tosilate (IPD) with chloride channels in human blood eosinophils: a potential mechanism underlying its anti-allergic and anti-asthmatic effects.
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Interaction of suplatast tosilate (IPD) with chloride channels in human blood eosinophils: a potential mechanism underlying its anti-allergic and anti-asthmatic effects.

机译：人体中嗜酸性粒细胞中磺基磺酸盐（IPD）与氯离子通道的相互作用：其抗过敏和抗哮喘作用的潜在机制。

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INTRODUCTION: Alterations in chloride ion channels have been implicated in the induction of changes in cell shape and volume. Because blood and tissue eosinophilia are hallmarks of bronchial asthma, in this study we examined the role of chloride channels in the underlying effects of suplatast tosilate (IPD), an anti-allergic drug, in human blood eosinophils. METHODS: Eosinophils were isolated and purified from the blood of allergic asthmatic donors. Chloride ion currents were recorded using the whole-cell patch-clamp technique in freshly isolated eosinophils. The current-voltage relationship of whole-cell currents in human blood eosinophils was calculated and recorded. The effect of chloride channel blockers was examined on superoxide release, eosinophil chemotaxis as measured by the Boyden chamber, and eosinophil adhesion to endothelial cells. Radioligand binding studies with [3H]IPD and competition curves with chloride channel blockers were performed. RESULTS: IPD increased both inward and outward chloride currents in human blood eosinophils. IPD in 1 ng/mL did not have significant effect on chloride current. However, at 5 ng/mL IPD activated both outward and inward currents in human blood eosinophils. Chloride channel blockers inhibited IPD-induced respiratory burst in eosinophils, eosinophil chemotaxis, and eosinophil adhesion to endothelial cells. All these effects of IPD on chloride current and the resultant functional responses in human blood eosinophils were not due to its basic salt, p-toluenesulphonic acid monohydrate. Human blood eosinophils contained specific binding sites for [3H]IPD with K(D) and B(max) values of 187.7+/-105.8 nm and 58.7+/-18.7 fmol/10(6) cells, respectively. Both NPPB and DIDS competed, in a dose-dependent manner, for the specific binding of [3H]IPD in human blood eosinophils. CONCLUSION: These data suggest that the anti-allergic and anti-asthmatic effects of IPD could be due to its interaction with chloride channels in human blood eosinophils.
机译：简介：氯离子通道的改变与细胞形状和体积变化的诱导有关。由于血液和组织嗜酸性粒细胞增多症是支气管哮喘的标志，因此在本研究中，我们研究了氯通道在人类血液嗜酸性粒细胞中抗过敏药物suplateast tosilate（IPD）的潜在作用中的作用。方法：从过敏性哮喘供体的血液中分离纯化出嗜酸性粒细胞。使用全细胞膜片钳技术在新鲜分离的嗜酸性粒细胞中记录氯离子电流。计算并记录人血嗜酸性粒细胞中全细胞电流的电流-电压关系。检查了氯离子通道阻滞剂对超氧化物的释放，嗜酸性粒细胞趋化性（通过博登室测量）以及嗜酸性粒细胞对内皮细胞的粘附的影响。用[3H] IPD进行放射性配体结合研究，并用氯离子通道阻断剂进行竞争曲线。结果：IPD增加了人类血液嗜酸性粒细胞的内向和外向氯化物电流。 1 ng / mL的IPD对氯化物电流没有显着影响。但是，当浓度为5 ng / mL时，IPD激活了人类血液嗜酸性粒细胞的内向和外向电流。氯离子通道阻滞剂可抑制IPD诱导的嗜酸性粒细胞呼吸爆发，嗜酸性粒细胞趋化性和嗜酸性粒细胞粘附于内皮细胞。 IPD对氯化物电流的所有这些影响以及在人血嗜酸性粒细胞中产生的功能响应并不是由于其碱性盐，即对甲苯磺酸一水合物。人血嗜酸性粒细胞含有[3H] IPD的特异性结合位点，其K（D）和B（max）值分别为187.7 +/- 105.8 nm和58.7 +/- 18.7 fmol / 10（6）细胞。 NPPB和DIDS都以剂量依赖的方式竞争人血嗜酸性粒细胞中[3H] IPD的特异性结合。结论：这些数据表明IPD的抗过敏和抗哮喘作用可能是由于其与人血嗜酸性粒细胞中的氯离子通道相互作用所致。

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