Abstract
BackgroundThe life cycle of Plasmodium is complex, requiring invasion of two different hosts, humans and mosquitoes. In humans, initiation of an effective Th1 response during early infection is critical for the control of parasite multiplication. In mosquitoes, inhibition of the development of sexual-stage parasites interrupts the parasite transmission. In this study, we aim to investigate whether dietary supplementation of L-arginine (L-Arg) in mice affects Plasmodium yoelii 17XL (Py17XL) transmission in mosquitoes.MethodsBALB/c mice were orally administered with 1.5 mg/g L-Arg daily for 7 days and infected with Py17XL. The mRNA levels of inducible nitric oxide synthase (iNOS) and arginase 1 in spleen cells were determined by real-time RT-PCR. The amount of nitric oxide (NO) released by spleen cells in vitro was determined by the Griess method. The effect of L-Arg supplementation on subsequent development of P. yoelii gametocytes was evaluated by an in vitro ookinete culture assay and mosquito feeding assay.ResultsPretreatment of mice with L-Arg significantly increased the transcript level of iNOS in spleen cells and the amount of NO synthesized. Dietary L-Arg supplementation also significantly reduced the number of zygotes and ookinetes formed during in vitro culture and the number of oocysts formed on mosquito midguts after blood feeding.ConclusionsL-Arg enhances host immunity against blood-stage parasites as well as suppressing subsequent parasite development in mosquitoes. L-Arg as an inexpensive and safe supplement may be used as a novel adjunct treatment against malarial infection.
Highlights
The life cycle of Plasmodium is complex, requiring invasion of two different hosts, humans and mosquitoes
We have recently shown that supplementation of L-Arg promotes the maturation of dendritic cells and improves protective immunity during early-stage Plasmodium yoelii 17XL (Py17XL) infection [9]
We studied the effects of L-Arg supplementation on the transcript levels of two arginine-metabolizing enzymes nitric oxide synthase and arginase 1 (ARG1)
Summary
The life cycle of Plasmodium is complex, requiring invasion of two different hosts, humans and mosquitoes. Inhibition of the development of sexual-stage parasites interrupts the parasite transmission. Malaria is a serious vector-borne disease that accounts for over half a million deaths annually. This infection remains widespread throughout the tropics, and occurs in many temperate regions [1]. The parasites first multiply in the human liver and subsequently infect red blood cells. Medications are primarily directed against the blood-stage parasites to ameliorate the malaria symptoms, whereas transmission blocking strategies target the sexual stages such as gametocyte, zygote, and ookinete [3, 4]
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