Infection by malaria parasite changes mechanical properties of red blood cells (RBCs). Infected red blood cells (IRBCs) lose the deformability but also develop the ability to cytoadhere and rosetting. These outcomes can lead to microvascular blockage [1]. The stiffness of IRBCs [2] and its effects on the flow in micro channels [3] were studied with recent experimental techniques. The cytoadherence and rosetting properties of IRBCs have also been studied experimentally. The cytoadherence is mediated by the interaction of the parasite protein PfEMP1 with several endothelial adhesion molecules, such as CD36, intercellular adhesion molecule-1 (ICAM-1), P-selectin, and vascular cell adhesion molecule-1 (VCAM-1) [4]. In particular, the ligand-receptor interaction between PfEMP1 and CD36 shows tight adhesion [5]. Microvascular blockage may be a hemodynamic problem, involving the interactions between IRBCs, healthy RBCs (HRBCs) and endothelial cells (ECs) in flowing blood, but however experimental techniques have several limitations to this topic. First, it is still difficult to observe the RBC behavior interacting with many other cells even with the recent confocal microscopy. Second, the three-dimensional information on flow field is hardly obtained. Third, capillaries in human body are circular channels with complex geometry, but such complex channels cannot be created in micro scale. Instead, numerical modeling can overcome these problems. We presented a two-dimensional hemodynamic model involving adhesive interactions [6]. In this paper, we propose a three-dimensional model of the adhesive interactions for micro scale hemodynamics in malaria infection.
Neutrophil Migration across Tight Junctions Is Mediated by Adhesive Interactions between Epithelial Coxsackie and Adenovirus Receptor and a Junctional Adhesion Molecule-like Protein on Neutrophils
