Ultrastructural Aspects of Plasmodium falciparum-Infected Erythrocyte Adherence to Endothelial Cells of Saimiri Brain Microvasculature

Robert, Claire; Peyrol, S; Pouvelle, Bruno; Gay-Andrieu, Françoise; Gysin, Jürg

doi:10.4269/ajtmh.1996.54.169

Cited by 14 publications

(6 citation statements)

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“…Monocyte pseudopodia could be seen contacting PRBC surfaces via electron-dense knobs, but this did not seem to be accompanied by active phagocytosis. Contact with PRBCs has been shown to affect the functions of other cells during adhesive events, including endothelial 14,34 and dendritic cells. 36 This emphasizes that PRBC adhesion is not a passive process, but can elicit functional and ultrastructural changes in host cells.…”

Section: Discussionmentioning

confidence: 99%

An Ultrastructural Study of the Brain in Fatal Plasmodium Falciparum Malaria

Pongponratn

Turner²,

Day³

et al. 2003

The American Journal of Tropical Medicine and Hygiene

204

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Cerebral malaria (CM) is a major cause of death in severe Plasmodium falciparum malaria. We present quantitative electron microscopic findings of the neuropathologic features in a prospective clinicopathologic study of 65 patients who died of severe malaria in Thailand and Vietnam. Sequestration of parasitized red blood cells (PRBCs) in cerebral microvessels was significantly higher in the brains of patients with CM compared with those with non-cerebral malaria (NCM) in all parts of the brain (cerebrum, cerebellum, and medulla oblongata). There was a hierarchy of sequestration with more in the cerebrum and cerebellum than the brain stem. When cerebral sequestration was compared with the peripheral parasitemia pre mortem, there were 26.6 times more PRBCs in the brain microvasculature than in the peripheral blood. The sequestration index was significantly higher in CM patients (median = 50.7) than in NCM patients (median = 6.9) (P = 0.042). The degree of sequestration of P. falciparum-infected erythrocytes in cerebral microvessels is quantitatively associated with pre-mortem coma.

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Section: Discussionmentioning

confidence: 99%

An Ultrastructural Study of the Brain in Fatal Plasmodium Falciparum Malaria

Pongponratn

Turner²,

Day³

et al. 2003

The American Journal of Tropical Medicine and Hygiene

204

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“…Ultrastructural studies of EC in human CM (52) have shown morphological changes of activation with membrane ruffling, lipid droplet accumulation and formation of pseudopodia which are seen to interact with host leukocytes and PRBC. Simian models of CM (53,76) have revealed the capacity of EC to phagocytose PRBC. Clearly the interaction of endothelial cells and parasitised erythrocytes and their role in transduction of stimuli to the brain microglia will be an important area of future research.…”

Section: The Neuropathology Of Malariamentioning

confidence: 99%

Cerebral Malaria

Turner

1997

Brain Pathology

154

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Malaria infection of the Central Nervous System (CNS) can cause a severe neurological syndrome termed Cerebral Malaria (CM). The central neuropathological feature of CM is the preferential sequestration of parasitised red blood cells (PRBC) in the cerebral microvasculature. The level of sequestration is related to the incidence of cerebral symptoms in severe malaria. Other neuropathological features of CM include petechial hemorrhages in the brain parenchyma, ring hemorrhages and Dürck's granuloma's. Immunohisto-chemical and electron microscopy studies have shown widespread cerebral endothelial cell activation and morphological changes occur in CM, as well as focal endothelial cell damage and necrosis. The immune cell response to intravascular sequestration appears to be limited, although activation of pigment-phagocytosing monocytes is a late feature. The mechanisms by which PRBC cause coma in malaria remain unclear. In vitro parasitised erythrocytes bind to endothelial cells by specific, receptor mediated interactions with host adhesion molecules such as ICAM-1, whose expression on cerebral endothelial cells is increased during CM as part of a systemic endothelial activation. Induction of local neuro-active mediators such as nitric oxide and systemic cytokines like TNF alpha may be responsible for the rapidly reversible symptoms of the coma of CM. The recent cloning of the parasite ligand PfEMP-1, thought to mediate binding to host sequestration receptors, promises further insight into the relationship between patterns of sequestration and the incidence and pathogenesis of coma in cerebral malaria.

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“…CSA was injected into monkeys infected with a Saimiri-adapted isolate of Palo-Alto (18). Splenectomized monkeys were used, because parasite sequestration does occur in splenectomized animals (13) and previously sequestered IRBCs remain in the circulation, as they are not destroyed by the spleen and are thus more readily detectable.…”

Section: Reversal Of Irbc Sequestration In Vivo By Inoculation Of Csamentioning

confidence: 99%