We show that ECM- resistant BALB/c mice were driven into interferon gamma- and IL-12-dependent ECM and subsequent death if they received CpG-oligonucleotides after Plasmodium berghei ANKA (PbA) infection.
Malaria-infection in mice results in a wide perturbation of the host serum proteome involving a range of proteins and functions.
To evaluate the accuracy in the oocyst counting with the improved technique, mosquitoes were infected with the green fluorescent protein (GFP)-expressing parasite.
Plasmodium berghei contained 0.454 ± 0.031 U/mg of glutathione synthetyase (GS). GS was purified using solid ammonium sulfate and Sephadex G-200 from P. berghei infected mouse erythrocytes.
The benzo[a]phenoxazine derivative, SSJ-183 has shown excellent anti-malarial efficacy and safety.
These results indicate that the protective effect of exogenous NO on murine CM is associated with decreased brain vascular expression of inflammatory markers resulting in attenuated endothelial junction damage and facilitating blood flow.
This study demonstrated the power of the transgenic P. berghei system to predict drug-resistant Pfdhfr mutations in an in vivo parasite/host setting.
Plasmodium infections are responsible for millions of cases of malaria and ∼1 million deaths annually.
These data indicate that CD8+ T cell-mediated immune pathology occurs in the brain but not the liver, while parasite-dependent pathology occurs in both organs during P. berghei ANKA infection.
In conclusion, this study contributes to the discovery of novel biomarkers in young susceptible rats and suggests that the decrease in their expression could be among the reasons for the development of severe pathology in malaria.
