New insights in intestinal ischemia-reperfusion injury: implications for intestinal transplantation.

K. Lenaerts, L.J. Ceulemans, I.H. Hundscheid, J. Grootjans, C.H.C. Dejong, S. Olde Damink

Research output: Contribution to journalArticleAcademicpeer-review

23 Citations (Scopus)

Abstract

Purpose of review

Ischemia-reperfusion injury is inevitable during intestinal transplantation and can negatively affect the transplant outcome. Here, an overview is provided of the recent advances in the pathophysiological mechanisms of intestinal ischemia-reperfusion injury and how this may impact graft survival.

Recent findings

The intestine hosts a wide range of microorganisms and its mucosa is heavily populated by immune cells. Intestinal ischemia-reperfusion results in the disruption of the epithelial lining, affecting also protective Paneth cells (antimicrobials) and goblet cells (mucus), and creates a more hostile intraluminal microenvironment. Consequently, both damage-associated molecular patterns as well as pathogen-associated molecular patterns are released from injured tissue and exogenous microorganisms, respectively. These 'danger' signals may synergistically activate the innate immune system. Exaggerated innate immune responses, involving neutrophils, mast cells, platelets, dendritic cells, as well as Toll-like receptors and complement proteins, may shape the adaptive T-cell response, thereby triggering the destructive alloimmune response toward the graft and resulting in transplant rejection.

Summary

Innate immune activation as a consequence of ischemia-reperfusion injury may compromise engraftment of the intestine. More dedicated research is required to further establish this concept in man and to design more effective therapeutic strategies to better tolerize intestinal grafts.

Original languageEnglish
Pages (from-to)298-303
Number of pages6
JournalCurrent Opinion in Organ Transplantation
Volume18
Issue number3
DOIs
Publication statusPublished - Jun 2013

Keywords

  • innate immune activation
  • intestine
  • ischemia-reperfusion
  • rejection
  • SOLID-ORGAN TRANSPLANTATION
  • ACUTE KIDNEY INJURY
  • ISCHEMIA/REPERFUSION INJURY
  • DENDRITIC CELLS
  • TISSUE-DAMAGE
  • CACO-2 CELLS
  • PANETH CELLS
  • ACTIVATION
  • GUT
  • INFLAMMATION

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