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Biology
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Neutrophil Extracellular Traps
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Neutrophil Extracellular Traps

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (15 October 2019) | Viewed by 19697

Special Issue Editor

Dr. Sebastian P. Galuska

E-Mail Website
Guest Editor
Leibniz Institute for Farm Animal Biology (FBN), Institute of Reproductive Biology, Wilhelm-Stahl-Allee 2, 18196 Dummerstorf, Germany
Interests: sialic acids; polysialic acid; glycoimmunology; siglecs; extracellular traps; innate immune system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As a part of the innate immune system, neutrophils play a key role during inflammation. An effective mechanism of these immune cells to counteract the invasion of pathogens is the reactive oxygen species (ROS)-dependent release of neutrophil extracellular traps (NETs). NET-fibers consist mainly of chromatin and granule proteins, which are released to trap and kill invaders. However, besides the positive outcomes of NETs, innumerable studies demonstrated that exaggerated NET-formation triggers several pathomechanisms, which can lead to life-threatening consequences like sepsis and thrombosis. Thus, not only the activation mechanisms, but also the modulation and inhibition of the release of NET are key points for the development of treatment strategies against such pathological situations.

This Special Issue is focused on the physiological and the pathophysiological roles of NETs in addition to the possibilities to modulate the activation of NET formation and the release of these NET fibers. This includes a comparison of NET mechanisms in different animal species forming a bridge between evolutionary biology and the biomedical sciences.

Dr. Sebastian P. Galuska
Guest Editor

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Keywords

  • neutrophils
  • extracellular traps
  • innate immune system
  • evolution

Published Papers (4 papers)

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Research

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19 pages, 3367 KiB  
Article
Histone H2A and Bovine Neutrophil Extracellular Traps Induce Damage of Besnoitia besnoiti-Infected Host Endothelial Cells but Fail to Affect Total Parasite Proliferation
by Iván Conejeros, Zahady D. Velásquez, Daniela Grob, Ershun Zhou, Hannah Salecker, Carlos Hermosilla and Anja Taubert
Biology 2019, 8(4), 78; https://doi.org/10.3390/biology8040078 - 11 Oct 2019
Cited by 20 | Viewed by 3226
Abstract
Besnoitia besnoiti tachyzoites infect and develop in bovine endothelial cells in vivo and trigger the release of neutrophil extracellular traps (NETs) from bovine polymorphonuclear neutrophils (PMN). The purpose of this study was to analyze if pure B. besnoiti tachyzoite-triggered NETs would damage endothelial [...] Read more.
Besnoitia besnoiti tachyzoites infect and develop in bovine endothelial cells in vivo and trigger the release of neutrophil extracellular traps (NETs) from bovine polymorphonuclear neutrophils (PMN). The purpose of this study was to analyze if pure B. besnoiti tachyzoite-triggered NETs would damage endothelial host cells and subsequently influence intracellular development and proliferation of B. besnoiti tachyzoites in primary bovine endothelial cells. For comparison purposes, isolated A23187-induced NETs were also used. Thus, we here evaluated endothelial host cell damage triggered by histone 2A (H2A) and B. besnoiti tachyzoite-induced NET preparations and furthermore estimated the effects of PMN floating over B. besnoiti-infected endothelium under physiological flow conditions on endothelial host cell viability. Overall, all treatments (H2A, B. besnoiti-triggered NETs and floating PMN) induced endothelial cell death of B. besnoiti-infected host cells. However, though host cell damage led to significantly altered intracellular parasite development with respect to parasitophorous vacuole diameter and numbers, the total proliferation of the parasite over time was not significantly affected by these treatments thereby denying any direct effect of NETs on intracellular B. besnoiti replication. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps)
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13 pages, 3248 KiB  
Article
Polysialic Acid Modulates the Binding of External Lactoferrin in Neutrophil Extracellular Traps
by Andrea Kühnle, Thomas Lütteke, Kim F. Bornhöfft and Sebastian P. Galuska
Biology 2019, 8(2), 20; https://doi.org/10.3390/biology8020020 - 28 Mar 2019
Cited by 13 | Viewed by 4636
Abstract
Neutrophil extracellular traps (NETs) are formed by neutrophils during inflammation. Among other things, these DNA constructs consist of antimicrobial proteins such as lactoferrin and histones. With these properties, NETs capture and destroy invading microorganisms. The carbohydrate polysialic acid (polySia) interacts with both lactoferrin [...] Read more.
Neutrophil extracellular traps (NETs) are formed by neutrophils during inflammation. Among other things, these DNA constructs consist of antimicrobial proteins such as lactoferrin and histones. With these properties, NETs capture and destroy invading microorganisms. The carbohydrate polysialic acid (polySia) interacts with both lactoferrin and histones. Previous experiments demonstrated that, in humans, lactoferrin inhibits the release of NET and that this effect is supported by polySia. In this study, we examined the interplay of lactoferrin and polySia in already-formed NETs from bovine neutrophils. The binding of polySia was considered to occur at the lactoferricin (LFcin)-containing domain of lactoferrin. The interaction with the peptide LFcin was studied in more detail using groups of defined polySia chain lengths, which suggested a chain-length-dependent interaction mechanism with LFcin. The LFcin domain of lactoferrin was found to interact with DNA. Therefore, the possibility that polySia influences the integration of lactoferrin into the DNA-structures of NETs was tested by isolating bovine neutrophils and inducing NETosis. Experiments with NET fibers saturated with lactoferrin demonstrated that polySia initiates the incorporation of external lactoferrin in already-loaded NETs. Thus, polySia may modulate the constituents of NET. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps)
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Review

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23 pages, 944 KiB  
Review
Extracellular Traps: An Ancient Weapon of Multiple Kingdoms
by Ariane Neumann, Graham Brogden and Maren von Köckritz-Blickwede
Biology 2020, 9(2), 34; https://doi.org/10.3390/biology9020034 - 18 Feb 2020
Cited by 32 | Viewed by 4791
Abstract
The discovery, in 2004, of extracellular traps released by neutrophils has extended our understanding of the mode of action of various innate immune cells. This fascinating discovery demonstrated the extracellular trapping and killing of various pathogens by neutrophils. During the last decade, evidence [...] Read more.
The discovery, in 2004, of extracellular traps released by neutrophils has extended our understanding of the mode of action of various innate immune cells. This fascinating discovery demonstrated the extracellular trapping and killing of various pathogens by neutrophils. During the last decade, evidence has accumulated showing that extracellular traps play a crucial role in the defence mechanisms of various cell types present in vertebrates, invertebrates, and plants. The aim of this review is to summarise the relevant literature on the evolutionary history of extracellular traps used as a weapon in various kingdoms of life. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps)
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17 pages, 1955 KiB  
Review
Pinniped- and Cetacean-Derived ETosis Contributes to Combating Emerging Apicomplexan Parasites (Toxoplasma gondii, Neospora caninum) Circulating in Marine Environments
by Rodolfo Villagra-Blanco, Liliana M. R. Silva, Iván Conejeros, Anja Taubert and Carlos Hermosilla
Biology 2019, 8(1), 12; https://doi.org/10.3390/biology8010012 - 09 Mar 2019
Cited by 22 | Viewed by 6348
Abstract
Leukocytes play a major role in combating infections either by phagocytosis, release of antimicrobial granules, or extracellular trap (ET) formation. ET formation is preceded by a certain leukocyte cell death form, known as ETosis, an evolutionarily conserved mechanism of the innate immune system [...] Read more.
Leukocytes play a major role in combating infections either by phagocytosis, release of antimicrobial granules, or extracellular trap (ET) formation. ET formation is preceded by a certain leukocyte cell death form, known as ETosis, an evolutionarily conserved mechanism of the innate immune system also observed in marine mammals. Besides several biomolecules and microbial stimuli, marine mammal ETosis is also trigged by various terrestrial protozoa and metazoa, considered nowadays as neozoan parasites, which are circulating in oceans worldwide and causing critical emerging marine diseases. Recent studies demonstrated that pinniped- and cetacean-derived polymorphonuclear neutrophils (PMNs) and monocytes are able to form different phenotypes of ET structures composed of nuclear DNA, histones, and cytoplasmic peptides/proteases against terrestrial apicomplexan parasites, e.g., Toxoplasma gondii and Neospora caninum. Detailed molecular analyses and functional studies proved that marine mammal PMNs and monocytes cast ETs in a similar way as terrestrial mammals, entrapping and immobilizing T. gondii and N. caninum tachyzoites. Pinniped- and cetacean leukocytes induce vital and suicidal ETosis, with highly reliant actions of nicotinamide adenine dinucleotide phosphate oxidase (NOX), generation of reactive oxygen species (ROS), and combined mechanisms of myeloperoxidase (MPO), neutrophil elastase (NE), and DNA citrullination via peptidylarginine deiminase IV (PAD4).This scoping review intends to summarize the knowledge on emerging protozoans in the marine environment and secondly to review limited data about ETosis mechanisms in marine mammalian species. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps)
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