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A High-throughput Assay to Assess and Quantify Neutrophil Extracellular Trap Formation
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A High-throughput Assay to Assess and Quantify Neutrophil Extracellular Trap Formation

Published on: January 29, 2019

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Uremic serum damages endothelium by provoking excessive neutrophil extracellular trap formation

Hoi Woul Lee1, Victor Nizet2, Jung Nam An3

  • 1Department of Clinical Immunology, Hallym University Sacred Heart Hospital, Anyang, South Korea.

Scientific Reports
|November 3, 2021
PubMed

Insights

Excessive neutrophil extracellular trap (NET) formation in chronic kidney disease (CKD) patients contributes to endothelial cell (EC) injury. Higher NET markers in hemodialysis patients predict mortality and vascular access failure, suggesting a role in cardiovascular disease.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Immunology

Background:

  • Cardiovascular disease (CVD) is the primary cause of death in chronic kidney disease (CKD) patients.
  • Endothelial cell (EC) dysfunction is a critical CKD-specific risk factor, but the underlying mechanisms remain unclear.
  • Uremia's impact on endothelial health is a significant concern in CKD management.

Purpose of the Study:

  • To investigate the role of excessive neutrophil extracellular trap (NET) formation in uremic serum-induced EC injury.
  • To evaluate plasma levels of NET markers (nucleosomes, myeloperoxidase-DNA) and ICAM-1 in hemodialysis (HD) patients.
  • To assess the prognostic significance of these markers for mortality and vascular access complications.

Main Methods:

  • Measured plasma nucleosome, myeloperoxidase-DNA, and ICAM-1 levels in incident HD patients and healthy volunteers (HV).
  • Conducted in vitro studies using HV-derived neutrophils and differentiated HL-60 cells exposed to uremic serum.
  • Assessed NET formation, EC viability, apoptosis, and levels of EC activation markers (ICAM-1, E-selectin, von Willebrand factor).

Main Results:

  • HD patients exhibited significantly higher in vivo NET markers and ICAM-1 levels compared to HV.
  • NET markers and ICAM-1 were strongly associated, with nucleosomes and ICAM-1 independently predicting mortality or vascular access failure.
  • Uremic serum significantly increased NET formation in vitro, leading to decreased EC viability, increased apoptosis, and elevated EC activation markers.

Conclusions:

  • Dysregulated neutrophil activity, specifically excessive NET formation, plays a key role in vascular inflammation in the uremic milieu.
  • Excessive NET formation contributes to EC damage and dysfunction, partially explaining the high mortality and CVD rates in end-stage renal disease (ESRD).
  • NETs represent a potential therapeutic target for mitigating cardiovascular risk in CKD patients.

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