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Zumstein, P.

Publications and source records attributed to Zumstein, P..

4 recordsLinked to original sources

Repurposing Niclosamide Ethanolamine for Alveolar Echinococcosis Reveals a Disconnect Between In Vitro Efficacy and In Vivo Outcome

BackgroundEchinococcosis is a zoonotic disease caused by cestodes of the genus Echinococcus. Alveolar echinococcosis (AE), caused by E. multilocularis, primarily affects the liver and shows infiltrative, tumor-like growth of the metacestode stage. If untreated, AE is lethal. AE remains a neglected disease with current treatments based on albendazole or mebendazole that are parasitostatic, and not curative, underscoring the need for more effective therapies. Niclosamide is a chlorinated salicylanilide derivative with proven activities against intestinal helminths but is inactive against tissue-dwelling helminths due to poor absorption and limited bioavailability. In this study, we repurposed niclosamide ethanolamine (NEN), a formulation with improved systemic exposure, for the treatment of E. multilocularis infection in vitro and in vivo. Methodology/Principal FindingsWe assessed the in vitro efficacy of niclosamide and NEN against E. multilocularis metacestode vesicles (IC50<0.2 {micro}M) and primary parasite cells (IC50<0.3 {micro}M), with active concentrations largely corresponding to NEN levels reachable in the liver. Metabolic analysis suggested that NEN acts as a mitochondrial uncoupler. Electron microscopy showed that NEN-treatments induced profound structural damage in the metacestode vesicle tissue, but mitochondrial ultrastructure was not notably affected. In mice intraperitoneally infected with E. multilocularis, NEN was orally administered during 9 weeks either alone, or in combination with albendazole. Pharmacokinetic analyses showed that NEN reached blood level concentrations above 1 {micro}M. However, the parasite burden in NEN-treated mice was not significantly reduced. Conclusions/SignificanceAlthough niclosamide and NEN demonstrated potent activity against E. multilocularis in vitro, this efficacy did not translate in the mouse model. The lack of in vivo activity could be attributed to several factors such as infection model, limited drug uptake by the parasite in the animal, or the rapid metabolization of the compound. Future studies should explore novel niclosamide derivatives and formulations to enhance efficacy against AE in vivo. Author SummaryAlveolar echinococcosis (AE) is a severe disease caused by the larval stage of the fox tapeworm Echinococcus multilocularis. The parasite forms tumor-like lesions in the liver and can spread to other organs. The currently licensed drugs for the treatment of AE are not always effective, require long-term use, and can cause side effects that frequently require treatment interruption. Therefore, safer and more efficacious treatment options are urgently needed. Niclosamide is frequently applied for the treatment of adult tapeworm infections in the intestine, but its limited uptake and low biodistribution renders the compound unsuitable for systemic treatment. In this study, we tested a non-toxic salt formulation, niclosamide ethanolamine (NEN), exhibiting improved absorption. In vitro, NEN was highly effective against E. multilocularis metacestode vesicles. It induced profound structural alterations in metacestode vesicles and impaired the mitochondrial membrane potential, and thus interfering in energy production. However, NEN was not effective against AE in experimentally infected mice. Our results suggest that NEN treatment appears promising in vitro, but to translate to the in vivo situation, new formulations and delivery strategies should be developed to increase absorption, bioavailability and metabolic stability of the compound for an effective treatment for AE.

pharmacology and toxicology↗

Triclabendazole inhibits succinate dehydrogenase in vitro

Succinate dehydrogenase (SDH, complex II), is essential for mitochondrial respiration. This study shows that triclabendazole and its primary metabolites inhibit SDH activity in mitochondria of the cestode Echinococcus multilocularis, while other tested benzimidazoles do not. Further analyses revealed that triclabendazole and metabolites also inhibit SDH in mitochondria of additional helminths (trematodes, nematodes) and mammalian cells. These findings indicate a shared mode of action and highlight potential safety risks associated with long-term triclabendazole treatment in mammals.

pharmacology and toxicology↗

Investigation of the threonine metabolism of Echinococcus multilocularis: the threonine dehydrogenase as a potential drug target in alveolar echinococcosis

Alveolar echinococcosis (AE) is a severe zoonotic disease caused by the metacestode stage of the fox tapeworm Echinococcus multilocularis. We recently showed that E. multilocularis metacestode vesicles scavenge large amounts of L-threonine from the culture medium that were neither stored nor overused for protein synthesis. This motivated us to study the effect of L-threonine on the parasite and how it is metabolized. We established a novel metacestode vesicle growth assay with an automated readout, which showed that L-threonine treatment led to significantly increased parasite growth. In addition, L-threonine increased the formation of novel metacestode vesicles from primary parasite cell cultures in contrast to the non-proteinogenic threonine analog 3-hydroxynorvaline. Tracing of [U-13C]-L-threonine and metabolites in metacestode vesicles and culture medium resulted in the detection of [U-13C]-labeling in aminoacetone and glycine, indicating that L-threonine was metabolized by threonine dehydrogenase (TDH). In addition, the detection of [13C2]-glutathione, suggested that E. multilocularis metacestode vesicles synthesize glutathione via L-threonine-derived glycine. EmTDH-mediated threonine metabolism in the E. multilocularis metacestode stage was further confirmed by quantitative real-time PCR, which demonstrated high expression of emtdh in in vitro cultured metacestode vesicles and also in metacestode samples obtained from infected animals. EmTDH was enzymatically active in metacestode vesicle extracts. Thus, the drugs disulfiram, myricetin, quercetin, sanguinarine and seven quinazoline carboxamides were assessed for inhibition of recombinantly expressed EmTDH, and the most potent inhibitors disulfiram, myricetin and sanguinarine were further tested for activity against E. multilocularis metacestode vesicles and primary parasite cells. Sanguinarine exhibited significant in vitro activity and IC50-values for metacestode vesicles, primary parasite cells, as well as mammalian cells were determined. Our results suggest that sanguinarine treatment should be further assessed in vivo employing suitable AE mouse models. Furthermore, the EmTDH assay could serve as high-throughput target-based discovery platform for novel anti-echinococcal compounds.

microbiology↗

Establishment and application of unbiased in vitro drug screening assays for the identification of compounds against Echinococcus granulosus s.s.

Echinococcus multilocularis and E. granulosus s.l. are the causative agents of alveolar and cystic echinococcosis, respectively. Drug treatment options for these severe and neglected diseases are limited to benzimidazoles, which are not always efficacious, and adverse side effects are reported. Thus, novel and improved treatments are needed. In this study, the previously established platform for E. multilocularis in vitro drug assessment was adapted to E. granulosus s.s.. In a first step, in vitro culture protocols for E. granulosus s.s. were established. This resulted in the generation of large amounts of E. granulosus s.s. metacestode vesicles as well as germinal layer (GL) cells. In vitro culture of these cells formed metacestode vesicles displaying structural characteristics of metacestode vesicles generated in vivo. Next, drug susceptibilities of E. multilocularis and E. granulosus s.s. protoscoleces, metacestode vesicles and GL cells were comparatively assessed employing established assays including (i) metacestode vesicle damage marker release assay, (ii) metacestode vesicle viability assay, (iii) GL cell viability assay, and (iv) protoscolex motility assay. The standard drugs albendazole, buparvaquone, mefloquine, MMV665807, monepantel, niclosamide and nitazoxanide were included. MMV665807, niclosamide and nitazoxanide were active against the parasite in all four assays against both species. MMV665807 and monepantel were significantly more active against E. multilocularis metacestode vesicles, while albendazole and nitazoxanide were significantly more active against E. multilocularis GL cells. Albendazole displayed activity against E. multilocularis GL cells, but no effects were seen in albendazole-treated E. granulosus s.s. GL cells within five days. Treatment of protoscoleces with albendazole and monepantel had no impact on motility. Similar results were observed for both species with praziquantel and its enantiomers against protoscoleces. In conclusion, in vitro culture techniques and drug screening methods previously established for E. multilocularis were successfully implemented for E. granulosus s.s., allowing comparisons of drug efficacy between the two species.

pharmacology and toxicology↗