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首页> 外文期刊>Infection and immunity >Shiga Toxin Binds Human Platelets via Globotriaosylceramide (Pk Antigen) and a Novel Platelet Glycosphingolipid
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Shiga Toxin Binds Human Platelets via Globotriaosylceramide (Pk Antigen) and a Novel Platelet Glycosphingolipid

机译：志贺毒素通过Globotriaosylceramide（Pk抗原）和新型血小板糖脂脂结合人血小板。

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Hemolytic-uremic syndrome is a clinical syndrome characterized by acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia that often follows infection by Shiga toxin- or verotoxin-producing strains of Escherichia coli. Because thrombocytopenia and platelet activation are hallmark features of hemolytic-uremic syndrome, we examined the ability of Shiga toxin to bind platelets by flow cytometry and high-performance thin-layer chromatography (HPTLC) of isolated platelet glycosphingolipids. By HPTLC, Shiga toxin was shown to bind globotriaosylceramide (Gb3) and a minor platelet glycolipid with anRf of 0.03, band 0.03. In a survey of 20 human tissues, band 0.03 was identified only in platelets. In individuals, band 0.03 was expressed by 20% of donors and was specifically associated with increased platelet Gb3 expression. Based on glycosidase digestion and epitope mapping, band 0.03 was hypothesized to represent a novel glycosphingolipid, IV3-β-Galα1-4galactosylglobotetraosylceramide. Based on incidence, structure, and association with increased Gb3 expression, band 0.03 may represent the antithetical Luke blood group antigen. By flow cytometry, Shiga toxin bound human platelets, although the amount of Shiga toxin bound varied in donors. Differences in Shiga toxin binding to platelet membranes did not reflect differences in platelet Gb3 expression. In contrast, there was a loose association between Shiga toxin binding and decreasing forward scatter, suggesting that Shiga toxin and verotoxins bind more efficiently to smaller, older platelets. In summary, Shiga and Shiga-like toxins may bind platelets via specific glycosphingolipid receptors. Such binding may contribute to the thrombocytopenia, platelet activation, and microthrombus formation observed in hemolytic-uremic syndrome.
机译：溶血尿毒症综合征是一种临床综合征，其特征在于急性肾衰竭，微血管病性溶血性贫血和血小板减少症，通常是由产志贺毒素或维毒素的大肠杆菌感染的。因为血小板减少症和血小板活化是溶血性尿毒症综合征的标志性特征，所以我们通过流式细胞术和分离的血小板糖鞘脂的高效薄层色谱法（HPTLC）检查了志贺毒素结合血小板的能力。通过HPTLC，志贺毒素显示出结合了globotriaosylceramide（Gb 3 ）和次要血小板糖脂，其中 R f 为0.03，带为0.03。在对20个人体组织的调查中，仅在血小板中发现了0.03带。在个体中，0.03条带由20％的供体表达，并与血小板Gb 3 表达增加有关。基于糖苷酶消化和表位作图，假设条带0.03代表新的糖鞘脂，IV 3 -β-Galα1-4半乳糖基球四糖基神经酰胺。根据发生率，结构以及与Gb 3 表达增加相关的关系，条带0.03可能代表了相对的Luke血型抗原。通过流式细胞术，志贺毒素结合人血小板，尽管供体中志贺毒素结合的量不同。志贺毒素与血小板膜结合的差异并不反映血小板Gb 3 表达的差异。相反，志贺毒素的结合与递减的前向散射之间存在松散的联系，表明志贺毒素和维毒素与更小，更老的血小板更有效地结合。总之，志贺和志贺样毒素可能通过特定的糖鞘脂受体结合血小板。这种结合可能有助于溶血性尿毒症综合征中观察到的血小板减少，血小板活化和微血栓形成。

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