Allicin could partially protect host against P. yoelii 17XL through enhancement of the host innate and adaptive immune responses.
Taken together, these results indicate that 1) P. yoelii gene expression remains stable in the presence of a changing host environment, and 2) concurrent expression of a large number of the polymorphic yir and pyst-a genes, rather than differential expression in response to specific host factors, may in itself limit the effectiveness of host immune responses.
L-arginine (L-Arg), the precursor of nitric oxide (NO), plays multiple important roles in nutrient metabolism and immune regulation.
In the present study, we found that 129S1 mice are resistant to the infection with Plasmodium yoelii 17XL, which is highly virulent and causes lethal infection in various strains of mice.
About 225 million malaria cases have been reported worldwide in 2009, and one-third of the world’s population is infected with parasitic helminths.
It is well established that CD4+CD25+Foxp3+ regulatory T cells (Tregs) play a crucial role in the course of different infectious diseases.
Macrophage migration inhibitory factor (MIF) has been shown to be involved in the pathogenesis of severe malaria.
Both P. yoelii 17XL and 17XNL strains could enhance the response of peritoneal macrophages to pRBC lysate and TLR agonists, through up-regulating the expression of TLR2 and intracellular signalling molecules MyD88, IRAK-1, and TRAF-6.
Of all the parasitic diseases, malaria is the number one killer.
The data clearly show that purinergic signalling modulates P. berghei protease(s) activity and that MSP1 is one target in this pathway.