Determination of lumefantrine as an effective drug against Toxoplasma gondii infection - in vitro and in vivo study

Toxoplasma gondii is an obligate intracellular protozoan parasite, which can infect almost all warm-blooded animals, including humans, leading to toxoplasmosis. Currently, the effective treatment for human toxoplasmosis is the combination of sulphadiazine and pyrimethamine. However, both drugs have serious side-effects and toxicity in the host. Therefore, there is an urgent need for the discovery of new anti-T. gondii drugs with high potency and less or no side-effects. Our findings suggest that lumefantrine exerts activity against T. gondii by inhibiting its proliferation in Vero cells in vitro without being toxic to Vero cells (P <= 0.01). Lumefantrine prolonged mice infected with T. gondii from death for 3 days at the concentration of 50 mu g L-1 than negative control (phosphate-buffered saline treated only), and reduced the parasite burden in mouse tissues in vivo (P <= 0.01; P <= 0.05). In addition, a significant increase in interferon gamma (IFN-gamma) production was observed in high-dose lumefantrine-treated mice (P <= 0.01), whereas interleukin 10 (IL-10) and IL-4 levels increased in low-dose lumefantrine-treated mice (P <= 0.01). The results demonstrated that lumefantrine may be a promising agent to treat toxoplasmosis, and more experiments on the protective mechanism of lumefantrine should be undertaken in further studies.

Automated summary

The study found that lumefantrine inhibits the proliferation of T. gondii in Vero cells without being toxic. In mice, lumefantrine at a concentration of 50 μg L-1 prolonged survival by 3 days and reduced parasite burden in tissues. High-dose lumefantrine increased IFN-γ production, while low-dose lumefantrine increased IL-10 and IL-4 levels in mice.