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Brain-Death in Rats Increases Neutrophil Extracellular Trap Formation in Donor Organs.

Maryna Van Zyl1,2, Roberto Armstrong Junior3, Petra Ottens3

  • 1Pathology Division, Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.

Transplant International : Official Journal of the European Society for Organ Transplantation
|May 7, 2025
PubMed
Summary

Neutrophil extracellular traps (NETs) are present in organs of brain-dead rats, contributing to inflammation and endothelial dysfunction. These findings suggest NETs play a role in organ injury following brain death.

Keywords:
brain-deathdonorendothelial activationneutrophil extracellular trapsneutrophils

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Area of Science:

  • Immunology
  • Pathology
  • Organ Transplantation

Background:

  • Brain death triggers an inflammatory response, recruiting neutrophils to organs.
  • Neutrophils may release neutrophil extracellular traps (NETs), potentially damaging organs and reducing quality.

Purpose of the Study:

  • To investigate the presence and role of NETs in organs from a rat model of brain death.
  • To determine if NETs contribute to endothelial activation, platelet infiltration, and oxidative stress.

Main Methods:

  • Collected kidneys, hearts, livers, and plasma from brain-dead and sham-operated rats.
  • Analyzed NETs, neutrophils, macrophages, and endothelial activation using immunofluorescence and immunohistochemistry.
  • Assessed platelet infiltration via qRT-PCR and systemic oxidative stress via plasma free thiol levels.

Main Results:

  • Increased neutrophils, NETs, and NET/neutrophil ratios were found in organs of brain-dead rats.
  • NETs positively correlated with endothelial cell activation.
  • Brain-dead rats exhibited increased macrophages, platelet infiltration, and systemic oxidative stress.

Conclusions:

  • NETs are present in organs from a brain-death donor model.
  • NETs, inflammation, and oxidative stress may contribute to endothelial dysfunction and organ injury during brain death.