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BACKGROUND: Patients in fulminant hepatic failure currently do not have a temporary means of support while awaiting liver transplantation. A potential therapeutic approach for such patients is the use of extracorporeal perfusion with porcine livers as a form of "liver dialysis". During a 72-h extracorporeal perfusion of porcine livers with human blood, porcine Kupffer cells bind to and phagocytose human red blood cells (hRBC) causing the hematocrit to decrease to 2.5% of the original value. Our laboratory has identified porcine sialoadhesin expressed on Kupffer cells as the lectin responsible for binding N-acetylneuraminic acid on the surface of the hRBC. We evaluated whether blocking porcine sialoadhesin prevents the recognition and subsequent destruction of hRBCs seen during extracorporeal porcine liver xenoperfusion. METHODS: Ex vivo studies were performed using wild type pig livers perfused with isolated hRBCs for 72-h in the presence of an anti-porcine sialoadhesin antibody or isotype control. RESULTS: The addition of an anti-porcine sialoadhesin antibody to an extracorporeal porcine liver xenoperfusion model reduces the loss of hRBC over a 72-h period. Sustained liver function was demonstrated throughout the perfusion. CONCLUSIONS: This study illustrates the role of sialoadhesin in mediating the destruction of hRBCs in an extracorporeal porcine liver xenoperfusion model.

Original publication

DOI

10.1111/xen.12043

Type

Conference paper

Publication Date

07/2013

Volume

20

Pages

239 - 251

Keywords

acute liver failure, adhesion molecules, hepatic failure, kupffer cells, liver assist/support, liver failure, liver support devices, macrophages, xenograft rejection, xenoperfusion, xenotransplantation, Animals, Antibodies, Anti-Idiotypic, Erythrocyte Transfusion, Erythrocytes, Extracorporeal Circulation, Humans, In Vitro Techniques, Kupffer Cells, Liver, Models, Animal, Perfusion, Phagocytosis, Sialic Acid Binding Ig-like Lectin 1, Swine, Time Factors, Transplantation, Heterologous