Small extracellular vesicles (sEVs), including exosomes, are formed by the endocytic pathway and contain genetic and protein material which reflect the contents of their cells of origin. These contents have a role in vesicle-mediated information transfer, as well as physiological and pathological functions. Thus, these vesicles are of great interest as therapeutic targets, or as vehicles for immunomodulatory control.
The transmission of Plasmodium spp. sporozoites to the mammalian host is the first step in the initiation of the mosquito-borne disease known as malaria. The exact route of transmission from the bloodstream to the liver is still not clearly elucidated, and identification of the host glycan structures bound by the sporozoites may inform as to which host cells are involved.
Plasmodium parasites cause malaria in mammalian hosts and are transmitted by Anopheles mosquitoes. Activated gametocytes in the mosquito midgut egress from erythrocytes followed by fertilization and zygote formation. Zygotes differentiate into motile invasive ookinetes, which penetrate the midgut epithelium before forming oocysts beneath the basal lamina.
Fixed-dose combination of artemisinin and naphthoquine (NQ) is a new artemisinin-based combination therapy for the treatment of uncomplicated Plasmodium falciparum. NQ absorption has been reported to be affected by food in human.
Sporozoites of the malaria parasite Plasmodium are transmitted by mosquitoes and infect the liver for an initial and obligatory round of replication, before exponential multiplication in the blood and onset of the disease. Sporozoites and liver stages provide attractive targets for malaria vaccines and prophylactic drugs. In this context, defining the parasite proteome is important to explore the parasite biology and to identify potential targets for antimalarial strategies. Previous studies have determined the total proteome of sporozoites from the two main human malaria parasites, P. falciparum and P. vivax, as well as P. yoelii, which infects rodents.
8-aminoquinoline compounds have long been the only therapeutic agents against latent hepatic malaria parasites. These have poor activity against the blood stage plasmodia causing acute malaria and must be used in conjunction with partner blood schizontocidal agents. We examined the impacts of one such agent, chloroquine, upon the activity of primaquine, an 8-aminoquinoline, against hepatic stages of Plasmodium cynomolgi, Plasmodium yoelii, Plasmodium berghei, and Plasmodium falciparum within several ex vivo systems: primary hepatocytes of Macaca fascicularis; primary human hepatocytes; and stably transformed human hepatocarcinoma cell line HepG2.
Cerebral malaria (CM) is one of the most severe pathologies of malaria; it induces neuro-cognitive sequelae and has a high mortality rate. Although many factors involved in the development of CM have been discovered, its pathogenic mechanisms are still not completely understood. Most studies on CM have focused on the blood-brain barrier (BBB), despite the importance of the blood-cerebrospinal fluid barrier (BCSFB), which protects the brain from peripheral inflammation.