Vibrio vulnificus hemolysin (VVH) is a pore-forming toxin secreted by Vibrio vulnificus. Cellular cholesterol was believed to be the receptor for VVH, because cholesterol could bind to VVH and preincubation with cholesterol inhibited cytotoxicity. It has been reported that specific glycans such as N-acetyl-D-galactosamine and N-acetyl-D-lactosamine bind to VVH, however, it has not been known whether these glycans could inhibit the cytotoxicity of VVH without oligomer formation. Thus, to date, binding mechanisms of VVH to cellular membrane, including specific receptors have not been elucidated. We show here that VVH associates with ganglioside GM1a, Fucosyl-GM1, GD1a, GT1c, and GD1b by glycan array. Among them, GM1a could pulldown VVH. Moreover, the GD1a inhibited the cytotoxicity of VVH without the formation of oligomers. This is the first report of a molecule able to inhibit the binding of VVH to target cells without oligomerization of VVH.

中文翻译：

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Vibiro vulnificus溶血素与神经节苷脂有关。

创伤弧菌溶血素（VVH）是由弧菌弧菌分泌的一种造孔毒素。细胞胆固醇被认为是VVH的受体，因为胆固醇可以与VVH结合并且与胆固醇预孵育抑制了细胞毒性。据报道，诸如N-乙酰基-D-半乳糖胺和N-乙酰基-D-乳糖胺之类的特定聚糖与VVH结合，但是，尚不清楚这些聚糖是否可以抑制VVH的细胞毒性而不形成低聚物。因此，迄今为止，尚未阐明VVH与细胞膜包括特定受体的结合机制。我们在这里显示VVH通过聚糖阵列与神经节苷脂GM1a，岩藻糖基GM1，GD1a，GT1c和GD1b缔合。其中，GM1a可以下拉VVH。此外，GD1a抑制VVH的细胞毒性而不形成寡聚物。