Rapid activation of endothelial cells enables Plasmodium falciparum adhesion to platelet-decorated von Willebrand factor strings

摘要: During Plasmodium falciparum malaria infections, von Willebrand factor (VWF) levels are elevated, postmortem studies show platelets colocalized with sequestered infected erythrocytes (IEs) at brain microvascular sites, whereas in vitro have demonstrated platelet-mediated IE adhesion to tumor necrosis factor-activated endothelium via a bridging mechanism. This current study demonstrates how all these observations could be linked through completely novel mechanism whereby IEs adhere platelet decorated ultra-large VWF strings on activated endothelium. Using an laminar flow model, we tethering and firm of the specifically sites accumulation. We also that pro-adhesive state, capable supporting high binding within minutes induction, can removed action protease ADAMTS-13 (a disintegrin metalloproteinase thrombospondin type 1 motif, member 13). propose this new contributes sequestration both independently concert mechanisms.