Inhibition of apoptosis reduces immunogeneic potential of adenoviral-treated syngeneic liver grafts

Puellmann, Kerstin and Beham, Alexander and Kienle, Klaus and Vogel, Mandy and Schlitt, Hans Juergen and Jauch, Karl Walter and Rentsch, Markus (2006) Inhibition of apoptosis reduces immunogeneic potential of adenoviral-treated syngeneic liver grafts. TRANSPLANTATION, 82 (10). pp. 1377-1382. ISSN 0041-1337,

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Abstract

Effects of adenoviral therapy and reduced apoptosis on immune response were investigated in a rat liver transplantation model after prolonged ischemia-reperfusion. Liver donors were treated i.v. either with an adenoviral construct, expressing bcl-2, green-fluorescent-protein, or doxycyclin. Intrahepatic apoptosis was assessed by terminal transferase dUTP nick end labeling assay. The intrahepatic presence of CD4, CD8a, CD163, immunoglobulin (1g)p, tumor necrosis factor (TNF)-alpha and myeloperoxidase (MPO) was quantified by realtime polymerase chain reaction at 24 hours and seven days after transplantation. Bcl-2 expression abrogated the TNF-alpha elevation and reduced apoptosis of hepatocytes and sinusoidal endothelial cells as compared to advCMV green fluorescent protein. No effects on CD4, CD8a, CD 163 and MPO expression were noticed in bd-2 pretreated livers, whereas Igo was slightly enhanced compared to controls. Adenoviral infected liver grafts trigger an immune response but reduced apoptosis resulted in down-regulation of TNF-alpha. Thus, bd-2 transfer might simultaneously reduce graft ischemia reperfusion injury and immunogenicity.

Item Type: Article
Uncontrolled Keywords: GENE-TRANSFER; IN-VIVO; INJURY; EXPRESSION; VECTORS; CELLS; RAT; TRANSPLANTATION; REPERFUSION; ISCHEMIA; liver transplantation; rat; bcl-2; adenovirus; graft survival; apoptosis
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Chirurgie
Medicine > Lehrstuhl für Innere Medizin II
Depositing User: Dr. Gernot Deinzer
Date Deposited: 18 Jan 2021 09:28
Last Modified: 18 Jan 2021 09:29
URI: https://pred.uni-regensburg.de/id/eprint/33748

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