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Recent Advances in Neutrophil Extracellular Traps (NETs)

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 613

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Guest Editor
1. Department of Pediatric Surgery, University Medical Center Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany
2. Department of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany
Interests: immunomodulation; neutrophil extracellular traps; NETs; CAR T-cells; pediatric tumor
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Dear Colleagues,

Neutrophils are the most abundant type of immune cells and are recruited into injured areas, remaining the dominant cell population for about two days. In response to infection and/or injury, neutrophils form neutrophil extracellular traps (NETs), which consist of double-stranded DNA filaments that are decorated with histones and cytotoxic proteins.

NETs are “double-edged swords” as they regulate homeostatic and pathological inflammation. During infection NETs exhibit antimicrobial functions, trapping and killing extracellular pathogens in blood and tissue. However, NETs also form during non-infectious inflammation. These NETs stimulate platelet adhesion and coagulation as well as inflammation. However, their aggregated form aids in the resolution of inflammation through histone-trapping and proteolytic activities.

While NETs play a pivotal role in combating infections and regulating inflammatory reactions, improper NET production can have adverse consequences. Indeed, research indicates that NETs contribute to the pathogenesis of various inflammatory conditions, including autoimmune diseases, wound healing, sepsis, tumor progression and ischemia-reperfusion injury. A common thread in these disorders is the participation of NETs in driving vascular occlusion and persistent hyperinflammation.

Prof. Dr. Michael Boettcher
Guest Editor

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  • neutrophils
  • neutrophil extracellular traps
  • NETs
  • inflammation
  • immunity

Published Papers (1 paper)

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20 pages, 18791 KiB  
The Dual Role of Neutrophil Extracellular Traps (NETs) in Sepsis and Ischemia-Reperfusion Injury: Comparative Analysis across Murine Models
by Antonia Kiwit, Yuqing Lu, Moritz Lenz, Jasmin Knopf, Christoph Mohr, Yannick Ledermann, Michaela Klinke-Petrowsky, Laia Pagerols Raluy, Konrad Reinshagen, Martin Herrmann, Michael Boettcher and Julia Elrod
Int. J. Mol. Sci. 2024, 25(7), 3787; https://doi.org/10.3390/ijms25073787 - 28 Mar 2024
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A better understanding of the function of neutrophil extracellular traps (NETs) may facilitate the development of interventions for sepsis. The study aims to investigate the formation and degradation of NETs in three murine sepsis models and to analyze the production of reactive oxygen [...] Read more.
A better understanding of the function of neutrophil extracellular traps (NETs) may facilitate the development of interventions for sepsis. The study aims to investigate the formation and degradation of NETs in three murine sepsis models and to analyze the production of reactive oxygen species (ROS) during NET formation. Murine sepsis was induced by midgut volvulus (720° for 15 min), cecal ligation and puncture (CLP), or the application of lipopolysaccharide (LPS) (10 mg/kg body weight i.p.). NET formation and degradation was modulated using mice that were genetically deficient for peptidyl arginine deiminase-4 (PAD4-KO) or DNase1 and 1L3 (DNase1/1L3-DKO). After 48 h, mice were killed. Plasma levels of circulating free DNA (cfDNA) and neutrophil elastase (NE) were quantified to assess NET formation and degradation. Plasma deoxyribonuclease1 (DNase1) protein levels, as well as tissue malondialdehyde (MDA) activity and glutathione peroxidase (GPx) activity, were quantified. DNase1 and DNase1L3 in liver, intestine, spleen, and lung tissues were assessed. The applied sepsis models resulted in a simultaneous increase in NET formation and oxidative stress. NET formation and survival differed in the three models. In contrast to LPS and Volvulus, CLP-induced sepsis showed a decreased and increased 48 h survival in PAD4-KO and DNase1/1L3-DKO mice, when compared to WT mice, respectively. PAD4-KO mice showed decreased formation of NETs and ROS, while DNase1/1L3-DKO mice with impaired NET degradation accumulated ROS and chronicled the septic state. The findings indicate a dual role for NET formation and degradation in sepsis and ischemia-reperfusion (I/R) injury: NETs seem to exhibit a protective capacity in certain sepsis paradigms (CLP model), whereas, collectively, they seem to contribute adversely to scenarios where sepsis is combined with ischemia-reperfusion (volvulus). Full article
(This article belongs to the Special Issue Recent Advances in Neutrophil Extracellular Traps (NETs))
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