Up-Regulation of ICAM-1 During Cold Ischemia Triggers Early Neutrophil Infiltration in Human Pancreas Allograft Reperfusion
| Autor: | Ernst Klar, Michael Linnebacher, Reiko Wiessner, Horst Nizze, S. Eisold, Rainer Wacke, C.M. Bünger, Wolfgang Schareck, Stefan Benz |
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| Rok vydání: | 2009 |
| Předmět: |
Adult
Male Pathology medicine.medical_specialty Neutrophils Biopsy medicine.medical_treatment Ischemia Granulocyte Pancreas transplantation Postoperative Complications Venules medicine Humans Transplantation Homologous Pancreas Transplantation business.industry Sodium Middle Aged Intercellular Adhesion Molecule-1 medicine.disease Capillaries Heart Arrest Up-Regulation P-Selectin medicine.anatomical_structure Reperfusion Injury Pancreatitis Female Surgery Pancreas Transplantation business Infiltration (medical) Reperfusion injury |
| Zdroj: | Transplantation Proceedings. 41:3622-3627 |
| ISSN: | 0041-1345 |
| Popis: | Graft pancreatitis is induced by ischemia/reperfusion injury in which neutrophil infiltration is believed to be a crucial early event. This observation suggests the presence of adhesion molecules already at the time of reperfusion. Therefore, this study was performed to evaluate the pattern of ICAM-1 and P-Selectin expression on human pancreas allografts following cold ischemia and reperfusion.We performed an analysis of pancreas biopsy specimens taken from 13 patients undergoing pancreas transplantation compared with pancreas specimens from 10 patients following resection. Cryostat sections were stained with monoclonal antibodies against CD11b, a neutrophil marker, and the adhesion molecules ICAM-1 and P-Selectin.Extensive infiltration of CD11b-positive cells was detected in venules and capillaries of pancreas allografts after reperfusion (18.38 +/- 0.87) compared with controls (T1 4.22 +/- 0.55) or with tissue specimens at about 10 hours of cold ischemia (2.60 +/- 0.35; P.001). Similarly, the pattern of P-Selectin showed a moderate expression before organ harvest (1.54 +/- 0.21) and in samples during cold ischemia (1.46 +/- 0.24) followed by a significantly greater number of P-Selectin-positive cells after reperfusion (2.54 +/- 0.18; P = .005). ICAM-1 was only weakly expressed on the surface of the venular endothelium in all controls (0.77 +/- 0.12). In contrast to P-Selectin, ICAM-1 showed prominent up-regulation during cold ischemia (2.23 +/- 0.23; P.001) with no further increase after reperfusion (2.23 +/- 0.17).The data suggested that ICAM-1 was already up-regulated during cold ischemia, possibly representing the mechanism of early neutrophil infiltration observed in human pancreatic ischemia/reperfusion injury. |
| Databáze: | OpenAIRE |
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