Introduction

Coccidia parasites are important obligate intracellular pathogens that affect humans and animals. These parasites are defective in cholesterol de novo synthesis but vastly need this molecule for membrane biosynthesis and offspring formation. Therefore, cholesterol must be scavenged from host cells, mainly via extracellular LDL particles.

Methods

We studied the role of scavenger receptor B type I (SR-BI) in the development of fast (Toxoplasma gondii, Neospora caninum, Besnoitia besnoiti) and slow (Eimeria bovis and Eimeria arloingi) replicating coccidian species by estimating the effects of the SR-BI-specific blocker BLT-1 on parasite replication.

Results

Overall, BLT-1 treatments significantly inhibited replication of all 5 coccidian parasites here studied indicating a common SR-BI-related key mechanism during parasite proliferation. Moreover, BLT1-mediated blockage of SR-BI induced an enhancement of host cell lipid droplet abundance and neutral lipid content, thereby confirming the importance of this receptor in lipid metabolism. However, SR-BI gene transcription was not affected by T. gondii, N. caninum and B. besnoiti infections. Interestingly, BLT-1 treatment of infective stages reduced the invasive capacity of all fast-replicating parasites paralleled by a sustained increase in cytoplasmic Ca⁺⁺ levels.

Conclusions

In conclusion, the data suggest a conserved role of SR-BI in successful coccidian proliferation.

Larrazabal, C.; López-Osorio, S.; Velásquez, Z.D.; Hermosilla, C.; Taubert, A.; Silva, L.M.R. Thiosemicarbazone Copper Chelator BLT-1 Blocks Apicomplexan Parasite Replication by Selective Inhibition of Scavenger Receptor B Type 1 (SR-BI). Microorganisms 2021, 9, 2372. https://doi.org/10.3390/microorganisms9112372