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Neutrophil Extracellular Traps in Disease and Immunity

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A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 5318

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Special Issue Editor

Dr. Blake Cochran

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Guest Editor

School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia
Interests: immunology; cholesterol in the mechanisms of disease development and progression; neutrophils

Special Issue Information

Dear Colleagues,

Neutrophils are the most abundant circulating leukocyte. Whilst neutrophils were originally defined as a ‘professional phagocyte’, the discovery of neutrophil extracellular traps (NETs) and the characterization of NETosis as more than simply a form of ‘cellular suicide’ added a new level of complexity to the role that these cells play in disease and immunity.

Beyond their role in the direct killing of pathogens, NETs are pro-inflammatory and can act as a trigger to activate other immune cells, both those involved in innate and adaptive immunity, thereby leading to an inflammatory response. Unregulated NETosis has been linked to the pathogenesis of many diseases, including cardiovascular disease, sepsis, cancer, and several autoimmune conditions.

NETs contain a wide array of biologically active proteins that activate signaling pathways in many cell types, contributing both to disease progression and pathogenesis as well as the immunological role of NETs.

For this Special Issue, we encourage the submission of manuscripts on any aspect of NETs—from the biochemical pathways involved in their production and release from cells through to the important roles that NETs and NET-associated factors play in modulating disease and immunity.

Dr. Blake Cochran
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

NETs
NETosis
neutrophils
inflammation
autoimmunity
cardiovascular disease
cancer
arthritis

Published Papers (3 papers)

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Research

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16 pages, 4296 KiB

Open AccessArticle

Insulin Can Delay Neutrophil Extracellular Trap Formation In Vitro—Implication for Diabetic Wound Care?

by Caren Linnemann, Filiz Şahin, Ningna Li, Stefan Pscherer, Friedrich Götz, Tina Histing, Andreas K. Nussler and Sabrina Ehnert

Biology 2023, 12(8), 1082; https://doi.org/10.3390/biology12081082 - 03 Aug 2023

Cited by 1 | Viewed by 1438

Abstract

Diabetes is a worldwide evolving disease with many associated complications, one of which is delayed or impaired wound healing. Appropriate wound healing strongly relies on the inflammatory reaction directly after injury, which is often altered in diabetic wound healing. After an injury, neutrophils are the first cells to enter the wound site. They have a special defense mechanism, neutrophil extracellular traps (NETs), consisting of released DNA coated with antimicrobial proteins and histones. Despite being a powerful weapon against pathogens, NETs were shown to contribute to impaired wound healing in diabetic mice and are associated with amputations in diabetic foot ulcer patients. The anti-diabetic drugs metformin and liraglutide have already been shown to regulate NET formation. In this study, the effect of insulin was investigated. NET formation after stimulation with PMA (phorbol myristate acetate), LPS (lipopolysaccharide), or calcium ionophore (CI) in the presence/absence of insulin was analyzed. Insulin led to a robust delay of LPS- and PMA-induced NET formation but had no effect on CI-induced NET formation. Mechanistically, insulin induced reactive oxygen species, phosphorylated p38, and ERK, but reduced citrullination of histone H3. Instead, bacterial killing was induced. Insulin might therefore be a new tool for the regulation of NET formation during diabetic wound healing, either in a systemic or topical application. Full article

(This article belongs to the Special Issue Neutrophil Extracellular Traps in Disease and Immunity)

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13 pages, 3924 KiB

Open AccessArticle

High-Throughput Analysis of Neutrophil Extracellular Trap Levels in Subtypes of People with Type 1 Diabetes

by Samal Bissenova, Mijke Buitinga, Markus Boesch, Hannelie Korf, Kristina Casteels, An Teunkens, Chantal Mathieu and Conny Gysemans

Biology 2023, 12(6), 882; https://doi.org/10.3390/biology12060882 - 19 Jun 2023

Cited by 1 | Viewed by 1570

Abstract

Neutrophils might play an important role in the pathogenesis of autoimmune diseases, including type 1 diabetes (T1D), by contributing to immune dysregulation via a highly inflammatory program called neutrophil extracellular trap (NET) formation or NETosis, involving the extrusion of chromatin entangled with anti-microbial proteins. However, numerous studies reported contradictory data on NET formation in T1D. This might in part be due to the inherent heterogeneity of the disease and the influence of the disease developmental stage on neutrophil behavior. Moreover, there is a lack of a standardized method to measure NETosis in an unbiased and robust manner. In this study, we employed the Incucyte^® ZOOM live-cell imaging platform to study NETosis levels in various subtypes of adult and pediatric T1D donors compared to healthy controls (HC) at baseline and in response to phorbol–myristate acetate (PMA) and ionomycin. Firstly, we determined that the technique allows for an operator-independent and automated quantification of NET formation across multiple time points, which showed that PMA and ionomycin induced NETosis with distinct kinetic characteristics, confirmed by high-resolution microscopy. NETosis levels also showed a clear dose-response curve to increasing concentrations of both stimuli. Overall, using Incucyte^® ZOOM, no aberrant NET formation was observed over time in the different subtypes of T1D populations, irrespective of age, compared to HC. These data were corroborated by the levels of peripheral NET markers in all study participants. The current study showed that live-cell imaging allows for a robust and unbiased analysis and quantification of NET formation in real-time. Peripheral neutrophil measures should be complemented with dynamic quantification of NETing neutrophils to make robust conclusions on NET formation in health and disease. Full article

(This article belongs to the Special Issue Neutrophil Extracellular Traps in Disease and Immunity)

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Review

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15 pages, 673 KiB

Open AccessReview

Immune Thrombosis: Exploring the Significance of Immune Complexes and NETosis

by José Perdomo and Halina H. L. Leung

Biology 2023, 12(10), 1332; https://doi.org/10.3390/biology12101332 - 12 Oct 2023

Cited by 2 | Viewed by 1810

Abstract

Neutrophil extracellular traps (NETs) are major contributors to inflammation and autoimmunity, playing a key role in the development of thrombotic disorders. NETs, composed of DNA, histones, and numerous other proteins serve as scaffolds for thrombus formation and promote platelet activation, coagulation, and endothelial dysfunction. Accumulating evidence indicates that NETs mediate thrombosis in autoimmune diseases, viral and bacterial infections, cancer, and cardiovascular disease. This article reviews the role and mechanisms of immune complexes in NETs formation and their contribution to the generation of a prothrombotic state. Immune complexes are formed by interactions between antigens and antibodies and can induce NETosis by the direct activation of neutrophils via Fc receptors, via platelet activation, and through endothelial inflammation. We discuss the mechanisms by which NETs induced by immune complexes contribute to immune thrombotic processes and consider the potential development of therapeutic strategies. Targeting immune complexes and NETosis hold promise for mitigating thrombotic events and reducing the burden of immune thrombosis. Full article

(This article belongs to the Special Issue Neutrophil Extracellular Traps in Disease and Immunity)

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