Bryan G. YippMichael J. HickeyGraciela AndoneguiAllan G. MurraySornchai LooareesuwanPaul KubesMay HoUniversity of CalgaryMonash UniversityUniversity of AlbertaMahidol University2018-08-242018-08-242007-08-01Microcirculation. Vol.14, No.6 (2007), 593-60215498719107396882-s2.0-34548128272https://repository.li.mahidol.ac.th/handle/20.500.14594/24158Cytoadherence of Plasmodium falciparum-infected red blood cells (IRBCs) on human microvascular endothelium is mediated by synergistic adhesive interactions with different adhesion molecules in vitro. Here, the authors used a unique human/severe combined immunodeficient (SCID) mouse chimeric model to directly visualize IRBC-endothelial interactions in an intact human microvasculature in vivo. Stimulation of human skin grafts with 100 ng TNF-α for 4 h led to a dramatic reduction in the distance rolled by IRBCs before arrest, so that the majority of IRBCs adhered directly to the endothelium with a 1.8-fold increase in the number of adherent cells. The decrease in rolling distance and increase in adhesion could be reversed by anti-ICAM-1. More importantly, the effect of TNF-α could be seen only in the presence of CD36. A further increase in adhesion by 4.9-fold was observed after 24 h of TNF-α stimulation. The increase could be reversed by anti-ICAM-1, but not anti-VCAM-1. In histamine-stimulated grafts, the rolling flux fraction and adhesion increased by 2.8- and 1.6-fold, respectively. The increases were attributable to P-selectin as an inhibitory anti-P-selectin antibody abrogated both the increased rolling flux fraction and firm adhesion. These findings indicate that in addition to CD36, ICAM-1, and P-selectin are major contributors to the dynamic process of IRBC adhesion by different mechanisms in vivo.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineArticleSCOPUS10.1080/10739680701404705