Variation in the cytoadherence characteristics of malaria parasites: is this a true virulence factor?

Abstract

The sequestration of Plasmodium falciparum-infected erythrocytes to the endothelial cells of brain capillaries is believed to represent one of the determining factors in the pathogenesis of cerebral malaria. In vitro studies of cytoadherence provide an experimental approach to understand the mechanism of sequestration and the respective roles played by parasite and host components in this interaction. This paper critically reviews current studies on cytoadherence, with particular emphasis on the nature of the information provided by such studies and their limitations. The paper also describes how cytoadherence studies using the patient's own monocytes can provide original information on the level of receptor up-regulation in the course of malarial infection.

Malaria rapid diagnostic tests: challenges and prospects

“…This enables the detection of PfHRP2 when sequestered parasites cannot be detected by microscopy. As P. falciparum parasites develop in the infected red blood cells from ring stage to trophozoites, they disappear from the peripheral circulation and cytoadhere to various organs in the host (MacPherson et al, 1985;Goldring et al, 1992;Goldring & Hommel, 1993;Goldring, 2004). PfHRP2 is found in the parasitophorous vacuole or in the parasite cytoplasm and the protein actively facilitates the polymerization of toxic haem, resulting from the degradation of host haemoglobin, to form a malaria pigment, haemozoin, which is no longer toxic (Sullivan et al, 1996).…”

Glucocorticoids, antioxidants and staurosporine modulate the adherence between monocytes and malaria infected erythrocytes

“…We have been studying the role monocyte adhesion molecules may have in malaria infections to understand the complex interactions between parasite, host, immunoregulation and drug therapy [3,4].…”

“…Malaria infected red cells have been shown to adhere to several receptors, including ICAM-1, vascular adhesion molecule-1 (VCAM-1), CD36 and E-selectin, [4,26,27] all of which are expressed by monocytes [28]. We have recently shown the down regulation of monocyte receptors to which malaria infected red cells attach in response to antimalarial drugs [29].…”