Screening the Global Health Priority Box Against Plasmodium berghei Liver Stage Parasites Using an Inexpensive Luciferase Detection Protocol

Author:

Nguyen Gia-Bao1,Cooper Caitlin A.1,McWhorter Olivia1,Sharma Ritu1,Elliot Anne1,Ruberto Anthony1,Cury Rafael1,Pathak Ashutosh K.1,Kyle Dennis E.1,Maher Steven P.1

Affiliation:

1. University of Georgia

Abstract

Abstract

Background Malaria, a disease caused by parasites of the genus Plasmodium, continues to impact many regions globally. The rise in resistance to artemisinin-based antimalarial drugs highlights the need for new treatments. Ideally, new antimalarials will kill the asymptomatic liver stages as well as the symptomatic blood stages. While blood stage screening assays are routine and efficient, liver stage screening assays are more complex and costly. To decrease the cost of liver stage screening we utilized a previously reported luciferase detection protocol requiring only common laboratory reagents and adapted this protocol for testing against luciferase-expressing Plasmodium berghei liver stage parasites. Methods After optimizing cell lysis conditions, the concentration of reagents, and the density of host hepatocytes (HepG2), we validated the protocol with 28 legacy antimalarials show this simple protocol produces a stable signal useful for obtaining quality small molecule potency data similar to that obtained from a high-content imaging endpoint. We then use the protocol to screen the Global Health Priority Box (GHPB) and confirm the potency of hits in dose-response assays. Selectivity was determined using a galactose-based, 72 hr HepG2 assay to avoid missing mitochondrial-toxic compounds due to the Crabtree effect. Receiver-operator characteristic plots were used to retroactively characterize the screens’ predictive value. Results Optimal luciferase signal was achieved using a lower HepG2 seed density (5 x 103 cells/well of a 384-well plate) compared to many previously-reported luciferase-based screens. While producing lower RLU’s compared to a commercial alternative, our luciferase detection method was found much more stable, with a > 3 hr half-life, and robust enough for producing dose-response plots with as few as 500 sporozoites/well. Our screen of the GHPB resulted in 9 hits with selective activity against P. berghei liver schizonts, including MMV674132 which exhibited 30.2 nM potency. Retrospective analyses show excellent predictive value for both antimalarial activity and cytotoxicity. Conclusions We project this method is suitable for high-throughput screening at a cost 20-fold less than using commercial luciferase detection kits, thereby enabling larger liver stage antimalarial screens and hit optimization make-test cycles. Further optimization of the hits detected using this protocol is ongoing.

Publisher

Springer Science and Business Media LLC

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