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Inhibition of human platelet aggregation by eosinophils

机译：嗜酸性粒细胞抑制人血小板聚集

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Aims The relationship between the activity of eosinophils and platelets has been observed in recent decades by many scientists. These observations include increased numbers of eosinophils associated with platelet disorders, including changes in the coagulation cascade and platelet aggregation. Based on these observations, the interaction between eosinophils and platelets in platelet aggregation was analyze. Main methods Human platelets were incubated with eosinophil cytosolic fraction, promyelocytic human HL-60 clone 15 cell lineage, and eosinophil cationic protein (ECP). Platelet rich plasma (PRP) aggregation was induced by adenosine diphosphate, platelet activating factor, arachidonic acid, and collagen, and washed platelets (WP) were activated by thrombin. Key findings Aggregation induced by all agonists was dose dependently inhibited by eosinophil cytosolic fraction. This inhibition was only partially reversed by previous incubation of the eosinophils with l-Nitro-Arginine-Methyl-Ester (l-NAME). Previous incubation with indomethacin did not prevent the cytosolic fraction induced inhibition. The separation of eosinophil cytosolic fraction by gel filtration on Sephadex G-75 showed that the inhibitory activity was concentrated in the lower molecular weight fraction. HL-60 clone 15 cells differentiated into eosinophils for 5 and 7 day were able to inhibit platelet aggregation. The ECP protein inhibited the platelet aggregation on PRP and WP. This inhibition was more evident in WP, and the citotoxicity MTT assay proved the viability of tested platelets, showing that the observed inhibition by the ECP protein does not occur simply by cell death. Significance Our results indicate that eosinophils play a fundamental role in platelet aggregation inhibition.
机译：目的近几十年来，许多科学家已观察到嗜酸性粒细胞活性与血小板之间的关系。这些观察结果包括与血小板疾病相关的嗜酸性粒细胞数量增加，包括凝血级联反应和血小板聚集的变化。基于这些观察，分析了嗜酸性粒细胞与血小板在血小板聚集中的相互作用。主要方法将人血小板与嗜酸性粒细胞胞质级分，早幼粒细胞人HL-60克隆15细胞谱系和嗜酸性粒细胞阳离子蛋白（ECP）一起孵育。二磷酸腺苷，血小板活化因子，花生四烯酸和胶原蛋白可诱导富含血小板的血浆（PRP）聚集，凝血酶可活化洗涤后的血小板（WP）。主要发现所有激动剂诱导的聚集被嗜酸性粒细胞胞质分数剂量依赖性抑制。通过先前将嗜酸性粒细胞与1-硝基-精氨酸-甲基-酯（1-NAME）一起温育，只能部分逆转这种抑制作用。先前与吲哚美辛孵育不会阻止胞质部分诱导的抑制作用。通过Sephadex G-75凝胶过滤分离嗜酸性粒细胞胞质部分，结果表明抑制活性集中在较低分子量部分。 HL-60克隆的15个细胞分化成嗜酸性粒细胞5天和7天能够抑制血小板聚集。 ECP蛋白抑制血小板在PRP和WP上的聚集。这种抑制作用在WP中更为明显，并且citotoxicity MTT分析证明了被测血小板的生存能力，表明观察到的ECP蛋白抑制作用并非仅因细胞死亡而发生。意义我们的结果表明，嗜酸性粒细胞在血小板聚集抑制中起着基本作用。

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