Plasmodium berghei ANKA: Erythropoietin activates neural stem cells in an experimental cerebral malaria model

2011 ◽  
Vol 127 (2) ◽  
pp. 500-505 ◽  
Author(s):  
Andrew Core ◽  
Casper Hempel ◽  
Jørgen A.L. Kurtzhals ◽  
Milena Penkowa
1998 ◽  
Vol 66 (9) ◽  
pp. 4093-4099 ◽  
Author(s):  
Véronique Amani ◽  
Mariama Idrissa Boubou ◽  
Sylviane Pied ◽  
Myriam Marussig ◽  
David Walliker ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e32048 ◽  
Author(s):  
Yuri C. Martins ◽  
Graziela M. Zanini ◽  
John A. Frangos ◽  
Leonardo J. M. Carvalho

1998 ◽  
Vol 66 (9) ◽  
pp. 4093-4099 ◽  
Author(s):  
Véronique Amani ◽  
Mariama Idrissa Boubou ◽  
Sylviane Pied ◽  
Myriam Marussig ◽  
David Walliker ◽  
...  

ABSTRACT Infection with Plasmodium berghei ANKA is usually lethal. The parasite causes in some mouse strains a neurovascular syndrome, experimental cerebral malaria (ECM), involving immunopathological reactions. The effects on the development of ECM of the mouse genetic background have been clearly demonstrated, but nothing is known about the effects of the clonal diversity of the parasite. We showed that various cloned lines derived from a polyclonal line of P. berghei ANKA caused ECM but that the extent of ECM induction was dependent on the amount of inoculum. Subtle differences in ECM characteristics (survival time and hypothermia) were also observed. We also confirmed, using the 1.49L cloned line, that the mouse genetic background strongly affects ECM.


2010 ◽  
Vol 78 (9) ◽  
pp. 4033-4039 ◽  
Author(s):  
Fernanda G. Baptista ◽  
Ana Pamplona ◽  
Ana C. Pena ◽  
Maria M. Mota ◽  
Sylviane Pied ◽  
...  

ABSTRACT Cerebral malaria is the most severe complication of human infection with Plasmodium falciparum. It was shown that Plasmodium berghei ANKA-induced cerebral malaria was prevented in 100% of mice depleted of CD8+ T cells 1 day prior to the development of neurological signs. However, the importance of parasites in the brains of these mice was never clearly investigated. Moreover, the relevance of this model to human cerebral malaria has been questioned many times, especially concerning the relative importance of leukocytes versus parasitized erythrocytes sequestered in the brain. Here, we show that mice protected from cerebral malaria by CD8+ T-cell depletion have significantly fewer parasites in the brain. Treatment of infected mice with an antimalarial drug 15 to 20 h prior to the estimated time of death also protected mice from cerebral malaria without altering the number of CD8+ T cells in the brain. These mice subsequently developed cerebral malaria with parasitized red blood cells in the brain. Our results clearly demonstrated that sequestration of CD8+ T cells in the brain is not sufficient for the development of cerebral malaria in C57BL/6 mice but that the concomitant presence of parasitized red blood cells is crucial for the onset of pathology. Importantly, these results also demonstrated that the experimental cerebral malaria model shares many features with human pathology and might be a relevant model to study its pathogenesis.


2018 ◽  
pp. 1
Author(s):  
سالم رمضان على السريتى ◽  
نوارة امراجع الازيرق العمارى

2013 ◽  
Vol 57 (7) ◽  
pp. 3412-3414 ◽  
Author(s):  
Jérome Dormoi ◽  
Sébastien Briolant ◽  
Camille Desgrouas ◽  
Bruno Pradines

ABSTRACTAlthough 100% of untreated mice infected withPlasmodium bergheidied with specific signs of cerebral malaria and 100% of mice treated with 3 mg/kg dihydroartemisinin, the active metabolite of artesunate, which is used as the first-line treatment for severe malaria, also died but showed no specific signs of cerebral malaria, 78% of mice treated with 10 mg/kg Proveblue (methylene blue) and 78% of mice treated with a combination of 3 mg dihydroartemisinin and 10 mg/kg Proveblue survived and showed no specific signs of cerebral malaria or detectable parasites.


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