Sterile Pancreas Inflammation during Preservation and after Transplantation

Abstract

The pancreas is very susceptible to ischemia-reperfusion injury. Early graft losses due to pancreatitis and thrombosis represent a major issue after pancreas transplantation. Sterile inflammation during organ procurement (during brain death and ischemia-reperfusion) and after transplantation affects organ outcomes. Sterile inflammation of the pancreas linked to ischemia-reperfusion injury involves the activation of innate immune cell subsets such as macrophages and neutrophils, following tissue damage and release of damage-associated molecular patterns and pro-inflammatory cytokines. Macrophages and neutrophils favor tissue invasion by other immune cells, have deleterious effects or functions, and promote tissue fibrosis. However, some innate cell subsets may promote tissue repair. This outburst of sterile inflammation promotes adaptive immunity activation via antigen exposure and activation of antigen-presenting cells. Better controlling sterile inflammation during pancreas preservation and after transplantation is of utmost interest in order to decrease early allograft loss (in particular thrombosis) and increase long-term allograft survival. In this regard, perfusion techniques that are currently being implemented represent a promising tool to decrease global inflammation and modulate the immune response.

Keywords: ischemia-reperfusion; pancreas; thrombosis; transplantation.

Figure 1

Inflammatory phenomena during pancreas transplantation and possible therapeutic interventions. IL interleukine, TNF tumor-necrosis factor, CCL2 chemokine ligand 2, MCP-1 monocyte chemoattractant protein 1, ATP adenosine tri-phosphate, ROS reactive oxygen species, HO-1 Heme oxygenase 1.