Cystic echinococcosis is caused by the larval stages (hydatids) of cestode parasites belonging to the species cluster Echinococcus granulosus sensu lato. 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 and draining lymph nodes in infected humans. These observations raise the question of whether LL materials circulate systemically, and if so how they are dealt with by the hosts. We previously reported that LL mucins are bound by a recombinant version of the lectin receptor Clec4F. In rodents, Clec4F is expressed only in Kupffer cells, the liver macrophages exposed to the vascular space. In this article, we show that Kupffer cells take up LL mucins in vivo in a manner dependent on the mucin glycans and Clec4F. In mice harbouring intraperitoneal infections, LL mucins were found essentially only at the infection site and in the liver, where they were taken up by Kupffer cells via Clec4F. It seems likely that the composition of the LL was adjusted through evolution so that LL debris were taken up by the major phagocytes of the rodent liver, which is the ancestral infection site for Echinococcus larvae. However, our data reveal that Kupffer cells act as a sink for LL materials even when the parasite grows in sites other than the liver, as it happens in natural E. granulosus infections.

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 bladderlike structures that attain large sizes within various internal organs of livestock ungulates and humans.