@article{oai:obihiro.repo.nii.ac.jp:00000834,
 author = {Nishikawa, Yoshifumi and 西川, 義文 and Ibrahim, Hany M. and Kameyama, Kyohko and Shiga, Ikumi and Hiasa, Jun and Xuan, Xuenan and 玄, 学南},
 issue = {5},
 journal = {Journal of Veterinary Medical Science},
 month = {},
 note = {application/pdf, The intracellular protozoan Toxoplasma gondii lacks the ability to synthesize sterol and scavenges cholesterol from the lowdensity
lipoprotein receptor (LDLR) pathway of its host to facilitate replication. Sterol biosynthesis inhibitors, however, have a demonstrated
anti-Toxoplasma effect. In this study, we examined the host mevalonate pathway as a novel source of cholesterol for T. gondii
and its effects on parasite growth in macrophages. Parasite growth did not significantly change in the absence of LDLR or when LDL
was exogenously supplemented. Lovastatin and compactin, both inhibitors of hydroxymethylglutaryl-CoA (HMG-CoA) reductase in the
mevalonate pathway, significantly inhibited T. gondii growth in both wild-type and LDLR-knockout macrophages. Parasite growth was
also suppressed by squalestatin, an inhibitor of squalene synthase, despite mevalonate producing isoprenoid intermediates in host cells.
The present study demonstrates that lovastatin, compactin and squalestatin have anti-Toxoplasma activities and that the host cholesterol
synthesis may contribute to parasite growth in macrophages.},
 pages = {633--639},
 title = {Host Cholesterol Synthesis Contributes to Growth of Intracellular Toxoplasma gondii in Macrophages},
 volume = {73},
 year = {2011}
}