Biology subjects

Barrios, A. A.

Publications and source records attributed to Barrios, A. A..

2 recordsLinked to original sources

bioRxiv2025

On the possible inhibition of macrophage inflammatory responses by phytic acid produced by Echinococcus multilocularis

Echinococcus multilocularis, causing agent of alveolar echinococcosis, down-regulates host immunity 1,2. Salzmann et al showed that macrophages close to the parasite produce little IL-6 and the parasite extract mimics this inhibition in cultured macrophages 3. The authors then showed that E. multilocularis contains phytic acid and that commercial phytic acid inhibits cytokine responses in stimulated macrophages. Through comparison with effects of EDTA and intracellular calcium measurements, they concluded that phytic acid inhibits macrophage responses through calcium depletion, extrapolating this conclusion to assays with parasite extract and infection setting. However, the interaction between phytic acid and calcium is complex 4,5. Calcium is indeed depleted in the assays with commercial phytic acid according to our quantitative predictions. However additional changes occur including formation of solid calcium phytate, which probably moderates the inhibition of responses observed under calcium depletion. We calculate that in the experiments with parasite extract, phytic acid present cannot deplete calcium and therefore inhibition must be driven by a different mechanism, possibly independent of phytic acid. Further, we argue that calcium depletion is an unlikely in vivo immune regulatory mechanism. We propose that biological assays using calcium phytate are needed for ascertaining whether phytic acid has biologically relevant anti-inflammatory activity.

immunology↗

bioRxiv2022

The lectin receptor Clec4F participates in the capture of circulating parasite mucins by Kupffer cells in cystic echinococcosis.

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.

immunology↗