Background

IgE to galactose alpha-1,3 galactose (alpha-gal) causes alpha-gal syndrome (delayed anaphylaxis after ingestion of mammalian meat). Development of sensitization has been attributed to tick bites; however, the possible role of other parasites has not been well studied.

Objective

Our aims were to assess the presence, relative abundances, and site of localization of alpha-gal–containing proteins in common ectoparasites and endoparasites endemic in an area of high prevalence of alpha-gal syndrome, as well as to investigate the ability of ascaris antigens to elicit a reaction in a humanized rat basophil in vitro sensitization model.

Methods

Levels of total IgE, Ascaris-specific IgE, and alpha-gal IgE were measured in sera from patients with challenge-proven alpha-gal syndrome and from controls without allergy. The presence, concentration, and localization of alpha-gal in parasites were assessed by ELISA, Western blotting, and immunohistochemistry. The ability of Ascaris lumbricoides antigen to elicit IgE-dependent reactivity was demonstrated by using the RS-ATL8 basophil reporter system.

Results

Alpha-gal IgE level correlated with A lumbricoides–specific IgE level. Alpha-gal protein at 70 to 130 kDa was detected in A lumbricoides at concentrations higher than those found in Rhipicephalus evertsi and Amblyomma hebraeum ticks. Immunohistochemistry was used to localize alpha-gal in tick salivary acini and the helminth gut. Non–alpha-gal–containing A lumbricoides antigens activated RS-ATL8 basophils primed with serum from subjects with alpha-gal syndrome.

Conclusion

We demonstrated the presence, relative abundances, and site of localization of alpha-gal–containing proteins in parasites. The activation of RS-ATL8 IgE reporter cells primed with serum from subjects with alpha-gal syndrome on exposure to non–alpha-gal–containing A lumbricoides proteins indicates a possible role of exposure to A lumbricoides in alpha-gal sensitization and clinical reactivity.

中文翻译：

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与半乳糖 α1,3-半乳糖致敏和引发 α-gal 综合征相关的蛔虫和蜱

背景

IgE 对半乳糖 alpha-1,3 半乳糖 (alpha-gal) 导致 alpha-gal 综合征（摄入哺乳动物肉类后的延迟性过敏反应）。过敏的发展归因于蜱叮咬；然而，其他寄生虫的可能作用尚未得到很好的研究。

客观的

我们的目的是评估在 α-gal 综合征高发地区流行的常见外寄生虫和内寄生虫中含 α-gal 蛋白的存在、相对丰度和定位位置，以及研究蛔虫抗原的能力在人源化大鼠嗜碱性粒细胞体外致敏模型中引发反应。

方法

在来自经攻击证实的 α-gal 综合征患者和没有过敏的对照的血清中测量总 IgE、蛔虫特异性 IgE 和 α-gal IgE 的水平。通过ELISA、蛋白质印迹和免疫组织化学评估寄生虫中α-gal的存在、浓度和定位。使用 RS-ATL8 嗜碱性粒细胞报告系统证明了蛔虫抗原引发 IgE 依赖性反应性的能力。

结果

Alpha-gal IgE 水平与A lumbricoides特异性 IgE 水平相关。在A lumbricoides中检测到 70 至 130 kDa 的 α-gal 蛋白，其浓度高于在Rhipicephalus evertsi和Amblyomma hebraeum蜱中发现的浓度。免疫组织化学用于定位蜱唾液腺泡和蠕虫肠道中的 α-gal。不含 α-gal 的A lumbricoides抗原激活 RS-ATL8 嗜碱性粒细胞，这些细胞用来自 α-gal 综合征受试者的血清引发。

结论

我们证明了寄生虫中含有 α-gal 的蛋白质的存在、相对丰度和定位位点。RS-ATL8 IgE 报告细胞在暴露于不含 α-gal 的 A lumbricoides 蛋白时，用来自患有 alpha-gal 综合征的受试者的血清激活，这表明暴露于A lumbricoides可能在 alpha-gal 致敏和临床反应中发挥作用。