Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines

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Author Spotlight: Neutrophil Extracellular Traps Imaging in Human and Mouse Tissues
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Author Spotlight: Neutrophil Extracellular Traps Imaging in Human and Mouse Tissues

Published on: August 18, 2023

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Christine Schauer1, Christina Janko2, Luis E Munoz1

  • 1Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.

Nature Medicine
|May 3, 2014
PubMed

Insights

Neutrophil extracellular traps (NETs) resolve gout inflammation by degrading inflammatory signals. Aggregated NETs, similar to tophi, are crucial for resolving acute gout and preventing chronic disease.

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Gout involves neutrophil accumulation and acute inflammation triggered by monosodium urate (MSU) crystals.
  • Inflammation typically resolves spontaneously, yet MSU crystals persist in tissues.
  • The resolution mechanism of gout inflammation remains incompletely understood.

Purpose of the Study:

  • To investigate the role of neutrophils and neutrophil extracellular traps (NETs) in gout inflammation resolution.
  • To explore the characteristics of aggregated NETs and their relationship to tophi.
  • To determine the impact of impaired NETosis on gout pathogenesis.

Main Methods:

  • Observation of neutrophil behavior and NET formation at inflammatory sites in gout models.
  • Analysis of aggregated NETs' structure and function, including cytokine degradation.
  • Induction of NETosis and aggregation using MSU crystals.
  • Assessment of gout models with impaired NETosis and rescue experiments using aggregated NETs.

Main Results:

  • Neutrophils form NETs during gout inflammation, which aggregate under high density.
  • Aggregated NETs degrade cytokines and chemokines via serine proteases, promoting inflammation resolution.
  • MSU crystals induce NETosis and NET aggregation, with impaired NETosis leading to persistent inflammation.
  • NETosis-deficient mice exhibited exacerbated chronic gout, ameliorated by aggregated NET transfer.

Conclusions:

  • Aggregated NETs play a critical role in resolving neutrophilic inflammation in gout.
  • NETosis and NET aggregation are key mechanisms for controlling inflammatory mediator production and neutrophil activity.
  • Targeting NET aggregation could offer therapeutic strategies for chronic gout and related inflammatory conditions.

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