An immunohistochemical study of the pathology of fatal malaria. Evidence for widespread endothelial activation and a potential role for intercellular adhesion molecule-1 in cerebral sequestration.

摘要: The sequestration of parasitized erythrocytes in the microvasculature vital organs is central to pathogenesis severe Plasmodium falciparum malaria. This process mediated by specific interactions between parasite adherence ligands and host receptors on vascular endothelium such as intercellular adhesion molecule-1 (ICAM-1) CD36. Using immunohistochemistry we have examined distribution putative different from fatal cases P. malaria noninfected controls. Receptor expression brain were quantified correlated. Fatal was associated with widespread induction endothelial activation markers, significantly higher levels ICAM-1 E-selectin vessels brain. In contrast, cerebral CD36 thrombospondin staining sparse, no evidence for increased There highly significant co-localization ICAM-1, CD36, but cellular inflammatory response. These results suggest that these a role vivo indicate systemic feature