The Effect of Anti ICAM-1 Antibody in the Rat Kidney Preserved in the Cold University of Wisconsin Solution / 대한이식학회지

ABSTRACT

PURPOSE: The cold ischemia augments the inflammatory cell infiltration in the rat kidney allograft by increasing expression of ICAM-1. The ICAM-1 proteins and ICAM-1 mRNA were overexpressed and upregulated on the tubular epithelium and endothelium of renal allografts that were preserved in the cold preservation solution such as University of Wisconsin (UW) solution. The aims of this study was to examine whether perfusion of kidney with anti ICAM-1 antibody (1A29) prevent inflammations and injuries of graft even in long ischemic time. METHODS: Rat kidneys were perfused in situ with 60 mL of cold UW solution without or with anti-rat ICAM-1 antibody and nephrectomized. The kidneys were exposed to 48 hour cold (4 degrees C storage time) ischemia and examined for the counts of necrotic tubules and apoptotic cells on the high power fields by terminal deoxynucleotidyltransferase mediated nick-end labeling (TUNEL) assay. RESULTS: The number of necrotic tubules per high power field of the allograft treated by anti ICAM-1antibody (6.97+/-4.25) was significantly less than that of the other control allograft (12.71+/-6.42) (P<0.001). The number of apoptotic cells per high power field of antibody treated graft (4.27+/-4.11) was significantly less than that of the other control graft (8.43+/-5.56) (P<0.001). CONCLUSION: Rat anti ICAM-1 antibody (1A29) inhibits ICAM-1 mediated allograft tubular necrosis as well as apoptosis. These results are expected to contribute to prevent allograft rejection and delayed graft function when used for pretreatment of allografts with anti ICAM-1 antibody mixtures of the perfusion and preserving solution clinically.