Mucins shed from the laminated layer in cystic echinococcosis are captured by Kupffer cells via the lectin receptor Clec4F
Mucins shed from the laminated layer in cystic echinococcosis are captured by Kupffer cells via the lectin receptor Clec4F
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DOI：
10.1101/2022.10.06.511139
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发表时间：
2023-03
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通讯作者：
A. A. Barrios-A.;Camila Mouhape;Leonard Schreiber;Linyun Zhang;J. Nell;Mariana Suárez-Martins;G. Schlapp;M. N. Meikle;A. P. Mulet;T. Hsu;Shie-Liang Hsieh;G. Mourglia-Ettlin;Carlos González;Martina Crispo;Thomas F. E. Barth;C. Casaravilla;Stephen J. Jenkins;Á. Díaz
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作者：
A. A. Barrios-A.;Camila Mouhape;Leonard Schreiber;Linyun Zhang;J. Nell;Mariana Suárez-Martins;G. Schlapp;M. N. Meikle;A. P. Mulet;T. Hsu;Shie-Liang Hsieh;G. Mourglia-Ettlin;Carlos González;Martina Crispo;Thomas F. E. Barth;C. Casaravilla;Stephen J. Jenkins;Á. Díaz
囊状棘球蚴病是由属于广义细粒棘球蚴属簇的绦虫寄生虫的幼虫阶段（包虫）引起的，其中E。严格意义上的粒层虫是主要的侵染种。棘球蚴是在家畜、有蹄类动物和人类的各种内部器官中获得大尺寸的囊状结构。包虫由主要由粘蛋白组成的大量非细胞层压层（LL）保护。寄生虫的生长需要LL营业额，和丰富的LL衍生的颗粒被发现在感染的人的感染部位，提出了如何处理的主机LL材料的问题。在这篇文章中，我们表明，E。注射到小鼠中的狭义颗粒状细胞LL粘蛋白被枯否细胞（暴露于血管空间的肝巨噬细胞）摄取。这种摄取在很大程度上依赖于完整的粘蛋白聚糖和Clec4F，Clec4F是一种C型凝集素受体，在啮齿动物中选择性地在枯否细胞中表达。这种摄取机制对以可溶性形式静脉注射和颗粒形式腹膜内注射的粘蛋白起作用。在同一种属的腹腔内感染小鼠中，LL粘蛋白基本上仅在感染部位和肝脏中发现，在那里它们通过Clec4F被枯否细胞吸收。因此，脱落的LL物质在宿主体内循环，枯否细胞可以作为这些物质的水槽，即使寄生虫在肝脏以外的部位生长。
Cystic echinococcosis is caused by the larval stages (hydatids) of cestode parasites belonging to the species cluster Echinococcus granulosus sensu lato, with E. granulosus sensu stricto being the main infecting species. Hydatids are bladder-like structures that attain large sizes within various internal organs of livestock ungulates and humans. Hydatids are protected by the massive acellular laminated layer (LL), composed mainly by mucins. Parasite growth requires LL turnover, and abundant LL-derived particles are found at infection sites in infected humans, raising the question of how LL materials are dealt with by the hosts. In this article, we show that E. granulosus sensu stricto LL mucins injected into mice are taken up by Kupffer cells, the liver macrophages exposed to the vascular space. This uptake is largely dependent on the intact mucin glycans and on Clec4F, a C-type lectin receptor which in rodents is selectively expressed in Kupffer cells. This uptake mechanism operates on mucins injected both in soluble form i.v. and in particulate form i.p. In mice harbouring intraperitoneal infections by the same species, LL mucins were found essentially only at the infection site and in the liver, where they were taken up by Kupffer cells via Clec4F. Therefore, shed LL materials circulate in the host and Kupffer cells can act as a sink for these materials even when the parasite grows in sites other than the liver.