Pathogenesis of cerebral malaria-inflammation and cytoadherence

被引:123
作者
Storm, Janet [1 ,2 ]
Craig, Alister G. [1 ]
机构
[1] Univ Liverpool, Liverpool Sch Trop Med, Dept Parasitol, Liverpool L3 5QA, Merseyside, England
[2] Univ Malawi, Coll Med, Malawi Liverpool Wellcome Trust Clini Res Program, Blantyre, Malawi
来源
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY | 2014年 / 4卷
基金
英国惠康基金;
关键词
cerebral malaria; endothelium dysfunction; inflammation; histopathology; PfEMP1; FALCIPARUM-INFECTED ERYTHROCYTES; PLASMODIUM-FALCIPARUM; NITRIC-OXIDE; ENDOTHELIAL ACTIVATION; PARASITE SEQUESTRATION; MALAWIAN CHILDREN; VAR GENES; MICROVASCULAR DYSFUNCTION; UNCOMPLICATED MALARIA; MOLECULAR-MECHANISMS;
D O I
10.3389/fcimb.2014.00100
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Despite decades of research on cerebral malaria (CM) there is still a paucity of knowledge about what actual causes CM and why certain people develop it. Although sequestration of P falciparum infected red blood cells has been linked to pathology, it is still not clear if this is directly or solely responsible for this clinical syndrome. Recent data have suggested that a combination of parasite variant types, mainly defined by the variant surface antigen, P falciparum erythrocyte membrane protein 1 (PfEMP1), its receptors, coagulation and host endothelial cell activation (or inflammation) are equally important. This makes CM a multi-factorial disease and a challenge to unravel its causes to decrease its detrimental impact.
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页数:8
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