Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
6.0
Journals
Cells
Special Issues
Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of...
share announcement

Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Intracellular and Plasma Membranes".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 23198

Special Issue Editors

Prof. Hans-Joachim Anders

E-Mail Website
Guest Editor
Division of Nephrology, Klinikum der Universitat Munchen, Munich, Germany
Interests: innate immunity; acute tissue injury; chronic tissue injjury; fibrosis; kidney disease; neutrophil extracellular traps; sterile inflammation; cell necrosis; necroinflammation; inflammasome; Toll-like receptors; regneration
Special Issues, Collections and Topics in MDPI journals
Dr. Shrikant R. Mulay

E-Mail Website
Guest Editor
Pharmacology Division, CSIR-Central Drug Research Institute, Lucknow, India
Interests: neutrophil extracellular traps; innate immunity; inflammation; regulated necrosis; acute kidney injury; chronic kidney diseases; crystallopathies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neutrophils are the most abundant leukocytes in human blood and have important roles in host defence and sterile inflammation. An absence of neutrophils or defects in neutrophil function, either inherited or acquired, is associated with immunodeficiency and autoimmunity, indicating the central role of neutrophils in health and disease. Neutrophil research has long focussed on granulopoiesis, phagocytosis, and degranulation, but since Zychlinsky et al. first reported the formation of neutrophil extracellular traps in 2004, this previously unrecognized effector function of neutrophils has attracted enormous attention in many specialist domains. Meanwhile, a role for neutrophil extracellular traps has been demonstrated in numerous disease contexts. Evolving new knowledge has been accompanied by numerous debates touching nomenclature; the significance of analytic assays; and data interpretation, a typical phenomenon in novel research domains. This Special Issue of Cells will create a forum to present and discuss new avenues in this expanding domain and will hopefully help to move the field forward towards a deeper understanding of the roles of neutrophil extracellular traps in health and disease. Therefore, we invite investigators to contribute original research, review, as well as opinion articles on this topic.

Prof. Hans-Joachim Anders
Prof. Shrikant R. Mulay
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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

  • neutrophil extracellular traps
  • infection
  • inflammation
  • thrombosis
  • autoimmunity
  • gout
  • sepsis
  • atherosclerosis
  • crystal

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review, Other

14 pages, 4554 KiB  
Article
Neutrophil Extracellular Traps Do Not Induce Injury and Inflammation in Well-Differentiated RSV-Infected Airway Epithelium
by Rosalie S. N. Linssen, Adithya Sridhar, Giulia Moreni, Nicole N. van der Wel, Job B. M. van Woensel, Katja C. Wolthers and Reinout A. Bem
Cells 2022, 11(5), 785; https://doi.org/10.3390/cells11050785 - 24 Feb 2022
Cited by 2 | Viewed by 2432
Abstract
Respiratory syncytial virus (RSV) lower respiratory tract infection (LRTI) causes a major burden of disease. The host response in RSV-LRTI is characterized by airway epithelial injury, inflammation and neutrophil influx, with the formation of neutrophil extracellular traps (NETs). However, the precise role of [...] Read more.
Respiratory syncytial virus (RSV) lower respiratory tract infection (LRTI) causes a major burden of disease. The host response in RSV-LRTI is characterized by airway epithelial injury, inflammation and neutrophil influx, with the formation of neutrophil extracellular traps (NETs). However, the precise role of NETs in the pathophysiology of RSV-LRTI remains to be elucidated. Here, we used well-differentiated human airway epithelial cultures (HAE) of a pediatric and adult donor to study whether NETs cause airway epithelial injury and inflammation in the setting of RSV infection. The exposure of uninfected and RSV-infected HAE cultures to NETs, as produced by stimulation of neutrophils by a low dose of phorbol 12-myristate 13-acetate (PMA), did not induce or aggravate cell injury or inflammation. RSV infection of HAE cultures caused release of pro-inflammatory cytokines such as IL-6 and RANTES in both adult and pediatric cultures, but the differential gene expression for regulated cell death differed between culture donors. In this in vitro airway epithelial model, NETs in the setting of RSV infection did not cause or aggravate epithelial injury or inflammation. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of Disease)
►▼ Show Figures

Figure 1

15 pages, 4304 KiB  
Article
An Imaging and Computational Algorithm for Efficient Identification and Quantification of Neutrophil Extracellular Traps
by Apurwa Singhal, Shubhi Yadav, Tulika Chandra, Shrikant R. Mulay, Anil Nilkanth Gaikwad and Sachin Kumar
Cells 2022, 11(2), 191; https://doi.org/10.3390/cells11020191 - 06 Jan 2022
Cited by 10 | Viewed by 3256
Abstract
Neutrophil extracellular traps (NETs) are associated with multiple disease pathologies including sepsis, asthma, rheumatoid arthritis, cancer, systemic lupus erythematosus, acute respiratory distress syndrome, and COVID-19. NETs, being a disintegrated death form, suffered inconsistency in their identification, nomenclature, and quantifications that hindered therapeutic approaches [...] Read more.
Neutrophil extracellular traps (NETs) are associated with multiple disease pathologies including sepsis, asthma, rheumatoid arthritis, cancer, systemic lupus erythematosus, acute respiratory distress syndrome, and COVID-19. NETs, being a disintegrated death form, suffered inconsistency in their identification, nomenclature, and quantifications that hindered therapeutic approaches using NETs as a target. Multiple strategies including microscopy, ELISA, immunoblotting, flow cytometry, and image-stream-based methods have exhibited drawbacks such as being subjective, non-specific, error-prone, and not being high throughput, and thus demand the development of innovative and efficient approaches for their analyses. Here, we established an imaging and computational algorithm using high content screening (HCS)—cellomics platform that aid in easy, rapid, and specific detection as well as analyses of NETs. This method employed membrane-permeable and impermeable DNA dyes in situ to identify NET-forming cells. Automated algorithm-driven single-cell analysis of change in nuclear morphology, increase in nuclear area, and change in intensities provided precise detection of NET-forming cells and eliminated user bias with other cell death modalities. Further combination with Annexin V staining in situ detected specific death pathway, e.g., apoptosis, and thus, discriminated between NETs, apoptosis, and necrosis. Our approach does not utilize fixation and permeabilization steps that disturb NETs, and thus, allows the time-dependent monitoring of NETs. Together, this specific imaging-based high throughput method for NETs analyses may provide a good platform for the discovery of potential inhibitors of NET formation and/or agents to modulate neutrophil death, e.g., NETosis-apoptosis switch, as an alternative strategy to enhance the resolution of inflammation. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of Disease)
►▼ Show Figures

Figure 1

Review

Jump to: Research, Other

15 pages, 20572 KiB  
Review
Neutrophil Extracellular Trap-Driven Occlusive Diseases
by Kursat Oguz Yaykasli, Christine Schauer, Luis E. Muñoz, Aparna Mahajan, Jasmin Knopf, Georg Schett and Martin Herrmann
Cells 2021, 10(9), 2208; https://doi.org/10.3390/cells10092208 - 26 Aug 2021
Cited by 14 | Viewed by 3886
Abstract
The enlightenment of the formation of neutrophil extracellular traps (NETs) as a part of the innate immune system shed new insights into the pathologies of various diseases. The initial idea that NETs are a pivotal defense structure was gradually amended due to several [...] Read more.
The enlightenment of the formation of neutrophil extracellular traps (NETs) as a part of the innate immune system shed new insights into the pathologies of various diseases. The initial idea that NETs are a pivotal defense structure was gradually amended due to several deleterious effects in consecutive investigations. NETs formation is now considered a double-edged sword. The harmful effects are not limited to the induction of inflammation by NETs remnants but also include occlusions caused by aggregated NETs (aggNETs). The latter carries the risk of occluding tubular structures like vessels or ducts and appear to be associated with the pathologies of various diseases. In addition to life-threatening vascular clogging, other occlusions include painful stone formation in the biliary system, the kidneys, the prostate, and the appendix. AggNETs are also prone to occlude the ductal system of exocrine glands, as seen in ocular glands, salivary glands, and others. Last, but not least, they also clog the pancreatic ducts in a murine model of neutrophilia. In this regard, elucidating the mechanism of NETs-dependent occlusions is of crucial importance for the development of new therapeutic approaches. Therefore, the purpose of this review is to address the putative mechanisms of NETs-associated occlusions in the pathogenesis of disease, as well as prospective treatment modalities. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of Disease)
►▼ Show Figures

Figure 1

29 pages, 2517 KiB  
Review
Contemporary Lifestyle and Neutrophil Extracellular Traps: An Emerging Link in Atherosclerosis Disease
by Laura Pérez-Olivares and Oliver Soehnlein
Cells 2021, 10(8), 1985; https://doi.org/10.3390/cells10081985 - 04 Aug 2021
Cited by 12 | Viewed by 4706
Abstract
Neutrophil extracellular traps (NETs) are networks of extracellular genetic material decorated with proteins of nuclear, granular and cytosolic origin that activated neutrophils expel under pathogenic inflammatory conditions. NETs are part of the host’s innate immune defense system against invading pathogens. Interestingly, these extracellular [...] Read more.
Neutrophil extracellular traps (NETs) are networks of extracellular genetic material decorated with proteins of nuclear, granular and cytosolic origin that activated neutrophils expel under pathogenic inflammatory conditions. NETs are part of the host’s innate immune defense system against invading pathogens. Interestingly, these extracellular structures can also be released in response to sterile inflammatory stimuli (e.g., shear stress, lipidic molecules, pro-thrombotic factors, aggregated platelets, or pro-inflammatory cytokines), as in atherosclerosis disease. Indeed, NETs have been identified in the intimal surface of diseased arteries under cardiovascular disease conditions, where they sustain inflammation via NET-mediated cell-adhesion mechanisms and promote cellular dysfunction and tissue damage via NET-associated cytotoxicity. This review will focus on (1) the active role of neutrophils and NETs as underestimated players of the inflammatory process during atherogenesis and lesion progression; (2) how these extracellular structures communicate with the main cell types present in the atherosclerotic lesion in the arterial wall; and (3) how these neutrophil effector functions interplay with lifestyle-derived risk factors such as an unbalanced diet, physical inactivity, smoking or lack of sleep quality, which represent major elements in the development of cardiovascular disease. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of Disease)
►▼ Show Figures

Figure 1

23 pages, 1124 KiB  
Review
A Fragile Balance: Does Neutrophil Extracellular Trap Formation Drive Pulmonary Disease Progression?
by Helena Block and Alexander Zarbock
Cells 2021, 10(8), 1932; https://doi.org/10.3390/cells10081932 - 29 Jul 2021
Cited by 23 | Viewed by 4712
Abstract
Neutrophils act as the first line of defense during infection and inflammation. Once activated, they are able to fulfil numerous tasks to fight inflammatory insults while keeping a balanced immune response. Besides well-known functions, such as phagocytosis and degranulation, neutrophils are also able [...] Read more.
Neutrophils act as the first line of defense during infection and inflammation. Once activated, they are able to fulfil numerous tasks to fight inflammatory insults while keeping a balanced immune response. Besides well-known functions, such as phagocytosis and degranulation, neutrophils are also able to release “neutrophil extracellular traps” (NETs). In response to most stimuli, the neutrophils release decondensed chromatin in a NADPH oxidase-dependent manner decorated with histones and granule proteins, such as neutrophil elastase, myeloperoxidase, and cathelicidins. Although primarily supposed to prevent microbial dissemination and fight infections, there is increasing evidence that an overwhelming NET response correlates with poor outcome in many diseases. Lung-related diseases especially, such as bacterial pneumonia, cystic fibrosis, chronic obstructive pulmonary disease, aspergillosis, influenza, and COVID-19, are often affected by massive NET formation. Highly vascularized areas as in the lung are susceptible to immunothrombotic events promoted by chromatin fibers. Keeping this fragile equilibrium seems to be the key for an appropriate immune response. Therapies targeting dysregulated NET formation might positively influence many disease progressions. This review highlights recent findings on the pathophysiological influence of NET formation in different bacterial, viral, and non-infectious lung diseases and summarizes medical treatment strategies. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of Disease)
►▼ Show Figures

Graphical abstract

Other

Jump to: Research, Review

8 pages, 241 KiB  
Brief Report
Neutrophil Extracellular Traps-DNase Balance and Autoimmunity
by Andrea Angeletti, Stefano Volpi, Maurizio Bruschi, Francesca Lugani, Augusto Vaglio, Marco Prunotto, Marco Gattorno, Francesca Schena, Enrico Verrina, Angelo Ravelli and Gian Marco Ghiggeri
Cells 2021, 10(10), 2667; https://doi.org/10.3390/cells10102667 - 05 Oct 2021
Cited by 24 | Viewed by 2988
Abstract
Neutrophil extracellular traps (NETs) are macromolecular structures programmed to trap circulating bacteria and viruses. The accumulation of NETs in the circulation correlates with the formation of anti-double-stranded (ds) DNA antibodies and is considered a causative factor for systemic lupus erythematosus (SLE). The digestion [...] Read more.
Neutrophil extracellular traps (NETs) are macromolecular structures programmed to trap circulating bacteria and viruses. The accumulation of NETs in the circulation correlates with the formation of anti-double-stranded (ds) DNA antibodies and is considered a causative factor for systemic lupus erythematosus (SLE). The digestion of DNA by DNase1 and DNases1L3 is the rate- limiting factor for NET accumulation. Mutations occurring in one of these two DNase genes determine anti-DNA formation and are associated with severe Lupus-like syndromes and lupus nephritis (LN). A second mechanism that may lead to DNase functional impairment is the presence of circulating DNase inhibitors in patients with low DNase activity, or the generation of anti-DNase antibodies. This phenomenon has been described in a relevant number of patients with SLE and may represent an important mechanism determining autoimmunity flares. On the basis of the reviewed studies, it is tempting to suppose that the blockade or selective depletion of anti-DNase autoantibodies could represent a potential novel therapeutic approach to prevent or halt SLE and LN. In general, strategies aimed at reducing NET formation might have a similar impact on the progression of SLE and LN. Full article
(This article belongs to the Special Issue Neutrophil Extracellular Traps: From Host Defence to the Pathophysiology of Disease)
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop