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包虫病(棘球蚴病)分层囊壁颗粒的急性炎症潜能受其六磷酸肌醇钙成分的调节。

The Acute Inflammatory Potential of Particles From the Echinococcus granulosus Laminated Layer Is Moderated by Its Calcium Inositol Hexakisphosphate Component.

机构信息

Área Inmunología, Departamento de Biociencias (Facultad de Química), Instituto de Higiene, Universidad de la República, Montevideo, Uruguay.

Laboratorio de Inmunología, Instituto de Química Biológica (Facultad de Ciencias), Instituto de Higiene, Universidad de la República, Montevideo, Uruguay.

出版信息

Parasite Immunol. 2024 May;46(5):e13040. doi: 10.1111/pim.13040.

DOI:10.1111/pim.13040
PMID:38801355
Abstract

Cystic echinococcosis is caused by the tissue-dwelling larva (hydatid) of Echinococcus granulosus sensu lato. A salient feature is that this larva is protected by the acellular laminated layer (LL). As the parasite grows, the LL sheds abundant particles that can accumulate in the parasite's vicinity. The potential of LL particles to induce inflammation in vivo has not been specifically analysed. It is not known how each of its two major components, namely highly glycosylated mucins and calcium inositol hexakisphosphate (InsP) deposits, impacts inflammation induced by the LL as a whole. In this work, we show that LL particles injected intraperitoneally cause infiltration of eosinophils, neutrophils and monocytes/macrophages as well as the disappearance of resident (large peritoneal) macrophages. Strikingly, the absence of calcium InsP enhanced the recruitment of all the inflammatory cell types analysed. In contrast, oxidation of the mucin carbohydrates caused decreased recruitment of neutrophils. The carbohydrate-oxidised particles caused cell influx nonetheless, which may be explained by possible receptor-independent effects of LL particles on innate immune cells, as suggested by previous works from our group. In summary, LL particles can induce acute inflammatory cell recruitment partly dependent on its mucin glycans, and this recruitment is attenuated by the calcium InsP component.

摘要

泡型包虫病是由细粒棘球绦虫(多房棘球绦虫亚种)的组织内幼虫(包虫)引起的。一个显著的特征是,这种幼虫被无细胞的层状层(LL)所保护。随着寄生虫的生长,LL 会脱落大量的颗粒,这些颗粒可以在寄生虫的附近积累。LL 颗粒在体内诱导炎症的潜力尚未被专门分析。目前尚不清楚其两个主要成分(即高度糖基化粘蛋白和肌醇六磷酸钙)中的每一个如何影响 LL 作为一个整体所引起的炎症。在这项工作中,我们表明,腹膜内注射 LL 颗粒会引起嗜酸性粒细胞、中性粒细胞和单核细胞/巨噬细胞的浸润,以及常驻(大腹膜)巨噬细胞的消失。引人注目的是,钙肌醇六磷酸的缺失增强了所有分析的炎症细胞类型的募集。相比之下,粘蛋白碳水化合物的氧化会导致中性粒细胞的募集减少。然而,碳水化合物氧化的颗粒仍然会引起细胞浸润,这可能是由于 LL 颗粒对先天免疫细胞的可能受体非依赖性影响,正如我们小组之前的工作所表明的那样。总之,LL 颗粒可以部分依赖于其粘蛋白糖来诱导急性炎症细胞募集,而这种募集会被钙肌醇六磷酸成分所减弱。

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