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Neutrophil Extracellular Traps: How to Generate and Visualize Them
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Neutrophil extracellular traps, damage-associated molecular patterns, and cell death during sepsis

Toshiaki Iba1, Miwa Murai1, Isao Nagaoka2

  • 1Department of Emergency and Disaster Medine Graduate School of Medicine, Juntendo University Tokyo Japan.

Acute Medicine & Surgery
|June 23, 2018
PubMed

Insights

Sepsis involves alarmins and damage-associated molecular patterns (DAMPs). Neutrophil extracellular traps (NETs), released during NETosis, trap microbes but can harm host cells, making their role in sepsis a key research area.

Area of Science:

  • Immunology
  • Cell Biology
  • Pathophysiology

Background:

  • Sepsis pathophysiology involves pathogen-associated molecular patterns and alarmins.
  • Damage-associated molecular patterns (DAMPs), including nucleosomes, histones, and DNA, define sepsis severity.
  • Neutrophil extracellular traps (NETs) represent a non-phagocytic antimicrobial mechanism.

Purpose of the Study:

  • To investigate the role of alarmins and DAMPs in sepsis.
  • To explore the mechanism and implications of NETosis in sepsis.
  • To understand the harmful effects of NETs on host cells during sepsis.

Main Methods:

  • Review of existing literature on sepsis, alarmins, DAMPs, and NETosis.
  • Analysis of the composition and function of neutrophil extracellular traps (NETs).
  • Discussion of the implications of NETosis in the context of sepsis pathophysiology.

Main Results:

  • NETs are composed of histones, DNA, and antimicrobial proteases like elastase and myeloperoxidase.
  • NETosis is a distinct cell death pathway crucial for trapping and eliminating microorganisms.
  • Released NETs can be harmful to host cells in circulating blood.

Conclusions:

  • Alarmins and DAMPs are critical in sepsis, alongside microbial components.
  • NETosis is a significant, albeit potentially harmful, host defense mechanism in sepsis.
  • Further research is needed to fully elucidate the multifaceted roles of NETs in sepsis.
Keywords:
Alarminhistoneinnate immune systemnecrosisneutrophil

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