| pubmed-article:8959777 | pubmed:abstractText | To investigate the effect of cytomegalovirus (CMV) infection on the development of experimental chronic kidney allograft rejection, orthotopic kidney allografts from DA donors (Ag-B4, RT1a1) to WF (Ag-B2, RT1u) recipients were used. The rats received cyclosporine A (CsA) for 12 weeks. A group of recipients was infected with 10(5) plaque-forming units of rat CMV (RCMV), and another group was left non-infected and used as controls. The grafts were removed 12 weeks after transplantation. RCMV infection significantly enhanced the development of chronic kidney allograft rejection as follows: the intensity of interstitial inflammation (P < 0.025), particularly the degree of pyroninophilic cells in the inflammatory infiltrate (P < 0.025); the glomeruli mesangial matrix increase (P < 0.05) and capillary basement membrane thickening (P < 0.01); the extent of endothelial cell swelling (P < 0.025) and intimal proliferation (P < 0.025) in the graft vasculature; and the extent of tubular epithelial atrophy (P < 0.025). The chronic allograft damage index (CADI) was significantly increased to 4.2 +/- 0.9 in RCMV-infected allografts, compared with 0.8 +/- 0.4 in non-infected (P < 0.02). At the molecular level, RCMV infection significantly increased vascular endothelial (P < 0.05) and tubular epithelial (P < 0.01) ICAM-1 expression. Viral antigens were detected in tubular epithelial cells and in some inflammatory cells. | lld:pubmed |
