BACKGROUND: Cytoadherence of Plasmodium falciparum-infected erythrocytes to host endothelium has been associated with pathology in severe malaria, but, despite extensive information on the primary processes involved in the adhesive interactions, the mechanisms underlying disease are poorly understood. METHODS: We compared parasite lines varying in their binding properties to human endothelial cells for their ability to stimulate signaling activity. RESULTS: In human umbilical vein endothelial cells (HUVECs), which rely on adhesion to intercellular adhesion molecule (ICAM)-1 for binding, signaling is related to the avidity of the parasite line for ICAM-1 and can be blocked either through the use of anti-ICAM-1 monoclonal antibodies or HUVECs with altered ICAM-1 binding properties (i.e., ICAM-1(Kilifi)). Human dermal microvascular endothelial cells (HDMECs), which can bind infected erythrocytes via ICAM-1 and CD36, have a more complex pattern of signaling behavior, but this is also dependent on adhesive interactions rather than merely contact between cells. CONCLUSIONS: Signaling via apposition of P. falciparum-infected erythrocytes with host endothelium is dependent, at least in part, on the cytoadherence characteristics of the invading isolate. An understanding of the postadhesive processes produced by cytoadherence may help us to understand the variable pathologies seen in malaria disease.
BACKGROUND: Cytoadherence of Plasmodium falciparum-infected erythrocytes to host endothelium has been associated with pathology in severe malaria, but, despite extensive information on the primary processes involved in the adhesive interactions, the mechanisms underlying disease are poorly understood. METHODS: We compared parasite lines varying in their binding properties to human endothelial cells for their ability to stimulate signaling activity. RESULTS: In human umbilical vein endothelial cells (HUVECs), which rely on adhesion to intercellular adhesion molecule (ICAM)-1 for binding, signaling is related to the avidity of the parasite line for ICAM-1 and can be blocked either through the use of anti-ICAM-1 monoclonal antibodies or HUVECs with altered ICAM-1 binding properties (i.e., ICAM-1(Kilifi)). Human dermal microvascular endothelial cells (HDMECs), which can bind infected erythrocytes via ICAM-1 and CD36, have a more complex pattern of signaling behavior, but this is also dependent on adhesive interactions rather than merely contact between cells. CONCLUSIONS: Signaling via apposition of P. falciparum-infected erythrocytes with host endothelium is dependent, at least in part, on the cytoadherence characteristics of the invading isolate. An understanding of the postadhesive processes produced by cytoadherence may help us to understand the variable pathologies seen in malaria disease.
Authors: Ziyue Lu; Lena Serghides; Samir N Patel; Norbert Degousee; Barry B Rubin; Gowdahali Krishnegowda; D Channe Gowda; Michael Karin; Kevin C Kain Journal: J Immunol Date: 2006-11-01 Impact factor: 5.422
Authors: Paco Pino; Ioannis Vouldoukis; Jean Pierre Kolb; Nassira Mahmoudi; Isabelle Desportes-Livage; François Bricaire; Martin Danis; Bernard Dugas; Dominique Mazier Journal: J Infect Dis Date: 2003-04-02 Impact factor: 5.226
Authors: Bryan G Yipp; Stephen M Robbins; Mary E Resek; Dror I Baruch; Sornchai Looareesuwan; May Ho Journal: Blood Date: 2002-11-27 Impact factor: 22.113
Authors: Michael A Krause; Seidina A S Diakite; Tatiana M Lopera-Mesa; Chanaki Amaratunga; Takayuki Arie; Karim Traore; Saibou Doumbia; Drissa Konate; Jeffrey R Keefer; Mahamadou Diakite; Rick M Fairhurst Journal: PLoS One Date: 2012-05-18 Impact factor: 3.240