scholarly journals Integrated inertial-impedance cytometry for rapid label-free leukocyte isolation and profiling of neutrophil extracellular traps (NETs)

Lab on a Chip ◽  
2019 ◽  
Vol 19 (10) ◽  
pp. 1736-1746 ◽  
Author(s):  
Chayakorn Petchakup ◽  
Hui Min Tay ◽  
King Ho Holden Li ◽  
Han Wei Hou
Keyword(s):  
Neutrophil Extracellular Traps ◽  
Neutrophil Extracellular Trap ◽  
Label Free ◽  
Extracellular Traps ◽  
Trap Formation ◽  
Extracellular Trap ◽  
Impedance Cytometry

A novel integrated inertial-impedance cytometer for rapid and label-free electrical profiling of neutrophil extracellular trap formation (NETosis).

scholarly journals Differential Use of Human Neutrophil FcγReceptors for Inducing Neutrophil Extracellular Trap Formation

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Omar Rafael Alemán ◽  
Nancy Mora ◽  
Ricarda Cortes-Vieyra ◽  
Eileen Uribe-Querol ◽  
Carlos Rosales
Keyword(s):  
Monoclonal Antibodies ◽  
Human Neutrophil ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Extracellular Trap ◽  
Cross Linking ◽  
Erk Activation ◽  
Extracellular Traps ◽  
Extracellular Trap ◽  
Antigen Antibody ◽  
Insight Into

Neutrophils (PMN) are the most abundant leukocytes in the blood. PMN migrate from the circulation to sites of infection, where they are responsible for antimicrobial functions. PMN use phagocytosis, degranulation, and formation of neutrophil extracellular traps (NETs) to kill microbes. NETs are fibers composed of chromatin and neutrophil-granule proteins. Several pathogens, including bacteria, fungi, and parasites, and also some pharmacological stimuli such as phorbol 12-myristate 13-acetate (PMA) are efficient inducers of NETs. Antigen-antibody complexes are also capable of inducing NET formation. However the particular Fcγreceptor involved in triggering this function is a matter of controversy. In order to provide some insight into what Fcγreceptor is responsible for NET formation, each of the two human Fcγreceptors was stimulated individually by specific monoclonal antibodies and NET formation was evaluated. FcγRIIa cross-linking did not promote NET formation. Cross-linking other receptors such as integrins also did not promote NET formation. In contrast FcγRIIIb cross-linking induced NET formation similarly to PMA stimulation. NET formation was dependent on NADPH-oxidase, PKC, and ERK activation. These data show that cross-linking FcγRIIIb is responsible for NET formation by the human neutrophil.

scholarly journals DNase I functional microgels for neutrophil extracellular trap disruption

2021 ◽  
Author(s):  
Aisa Hosseinnejad ◽  
Nadine Ludwig ◽  
Ann-Katrin Wienkamp ◽  
Rahul Rimal ◽  
Christian Bleilevens ◽  
...  
Keyword(s):  
Neutrophil Extracellular Traps ◽  
Dnase I ◽  
Neutrophil Extracellular Trap ◽  
Extracellular Traps ◽  
Extracellular Trap ◽  
Non Fouling

Non-fouling DNase I conjugated microgel provide a novel biohybrid platform to disrupt Neutrophil extracellular traps (NETs) and can be used as a non-thrombogenic coating for reduction of NET-mediated inflammation and microthrombi formation.

scholarly journals The emerging roles of neutrophil extracellular traps in wound healing

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Shuainan Zhu ◽  
Ying Yu ◽  
Yun Ren ◽  
Liying Xu ◽  
Huilin Wang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Healing Process ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Extracellular Trap ◽  
Wound Healing Process ◽  
Loss Of Function ◽  
Delayed Wound Healing ◽  
Wound Site ◽  
Extracellular Traps ◽  
Extracellular Trap

AbstractDelayed wound healing causes problems for many patients both physically and psychologically, contributing to pain, economic burden, loss of function, and even amputation. Although many factors affect the wound healing process, abnormally prolonged or augmented inflammation in the wound site is a common cause of poor wound healing. Excessive neutrophil extracellular trap (NET) formation during this phase may amplify inflammation and hinder wound healing. However, the roles of NETs in wound healing are still unclear. Herein, we briefly introduce NET formation and discuss the possible NET-related mechanisms in wound healing. We conclude with a discussion of current studies, focusing on the roles of NETs in diabetic and normoglycemic wounds and the effectiveness of NET-targeting treatments in wound healing.

scholarly journals Neutrophil extracellular traps and thrombosis in COVID-19

2020 ◽  
Author(s):  
Yu Zuo ◽  
Melanie Zuo ◽  
Srilakshmi Yalavarthi ◽  
Kelsey Gockman ◽  
Jacqueline A. Madison ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Histone H3 ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Extracellular Trap ◽  
Dna Complexes ◽  
Extracellular Traps ◽  
Free Dna ◽  
Extracellular Trap ◽  
Net Release ◽  
D Dimer

ABSTRACTHere, we report on four patients whose hospitalizations for COVID-19 were complicated by venous thromboembolism (VTE). All demonstrated high levels of D-dimer as well as high neutrophil-to-lymphocyte ratios. For three patients, we were able to test sera for neutrophil extracellular trap (NET) remnants and found significantly elevated levels of cell-free DNA, myeloperoxidase-DNA complexes, and citrullinated histone H3. Neutrophil-derived S100A8/A9 (calprotectin) was also elevated. Given strong links between hyperactive neutrophils, NET release, and thrombosis in many inflammatory diseases, the potential relationship between NETs and VTE should be further investigated in COVID-19.

scholarly journals On Neutrophil Extracellular Trap (NET) Removal: What We Know Thus Far and Why So Little

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2079
Author(s):  
Michal Santocki ◽  
Elzbieta Kolaczkowska
Keyword(s):  
Neutrophil Extracellular Traps ◽  
Therapeutic Strategies ◽  
Neutrophil Extracellular Trap ◽  
Know How ◽  
Extracellular Traps ◽  
Pathological Conditions ◽  
Extracellular Trap

Although neutrophil extracellular traps (NETs) were discovered only 16 years ago, they have already taken us from heaven to hell as we learned that apart from beneficial trapping of pathogens, they cause, or contribute to, numerous disorders. The latter is connected to their persistent presence in the blood or tissue, and we hardly know how they are removed in mild pathophysiological conditions and why their removal is impaired in multiple severe pathological conditions. Herein, we bring together all data available up till now on how NETs are cleared—from engaged cells, their phenotypes, to involved enzymes and molecules. Moreover, we hypothesize on why NET removal is challenged in multiple disorders and propose further directions for studies on NET removal as well as possible therapeutic strategies to have them cleared.

scholarly journals Neutrophil Extracellular Traps in Tumor Metastasis: Pathological Functions and Clinical Applications

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2832
Author(s):  
Qian Chen ◽  
Lu Zhang ◽  
Xiang Li ◽  
Wei Zhuo
Keyword(s):  
Tumor Metastasis ◽  
Immune Escape ◽  
Prognostic Biomarker ◽  
Neutrophil Extracellular Traps ◽  
Clinical Applications ◽  
Neutrophil Extracellular Trap ◽  
Pathogenic Microorganisms ◽  
Extracellular Traps ◽  
Extracellular Trap ◽  
Cell Malignancy

Neutrophil extracellular trap (NET) formation is an ability of neutrophils to capture and kill pathogens by releasing chromatin scaffolds, along with associated cytotoxic enzymes and proteases, into the extracellular space. NETs are usually stimulated by pathogenic microorganisms and their products, surgical pressure or hypoxia. Interestingly, a number of recent studies suggest that tumor cells can induce NET formation, which in turn confers tumor cell malignancy. Notably, emerging studies indicate that NETs are involved in enhancing local invasion, increasing vascular permeability and facilitating immune escape and colonization, thus promoting tumor metastasis. In this article, we review the pivotal roles of NETs in the tumor metastasis cascade. We also recapitulate the potential of NETs as a cancer prognostic biomarker and therapeutic target.

scholarly journals Neutrophil Extracellular Traps in Atherosclerosis and Thrombosis

2020 ◽  
Author(s):  
Thomas M. Hofbauer ◽  
Anna S. Ondracek ◽  
Irene M. Lang
Keyword(s):  
Innate Immunity ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Extracellular Trap ◽  
Neutrophil Granulocytes ◽  
Preventive Strategies ◽  
Extracellular Traps ◽  
Health Burden ◽  
Acute Complications ◽  
Extracellular Trap

AbstractDespite effective therapeutic and preventive strategies, atherosclerosis and its complications still represent a substantial health burden. Leukocytes and inflammatory mechanisms are increasingly recognized as drivers of atherosclerosis. Neutrophil granulocytes within the circulation were recently shown to undergo neutrophil extracellular trap (NET) formation, linking innate immunity with acute complications of atherosclerosis. In this chapter, we summarize mechanisms of NET formation, evidence for their involvement in atherosclerosis and thrombosis, and potential therapeutic regimens specifically targeting NET components.

scholarly journals Myeloperoxidase is required for neutrophil extracellular trap formation: implications for innate immunity

Blood ◽  
2011 ◽  
Vol 117 (3) ◽  
pp. 953-959 ◽  
Author(s):  
Kathleen D. Metzler ◽  
Tobias A. Fuchs ◽  
William M. Nauseef ◽  
Dominique Reumaux ◽  
Joachim Roesler ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Candida Albicans ◽  
Host Defense ◽  
Candida Species ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Extracellular Trap ◽  
Extracellular Traps ◽  
Microbial Infections ◽  
Dependent Inhibition ◽  
Extracellular Trap

AbstractThe granule enzyme myeloperoxidase (MPO) plays an important role in neutrophil antimicrobial responses. However, the severity of immunodeficiency in patients carrying mutations in MPO is variable. Serious microbial infections, especially with Candida species, have been observed in a subset of completely MPO-deficient patients. Here we show that neutrophils from donors who are completely deficient in MPO fail to form neutrophil extracellular traps (NETs), indicating that MPO is required for NET formation. In contrast, neutrophils from partially MPO-deficient donors make NETs, and pharmacological inhibition of MPO only delays and reduces NET formation. Extracellular products of MPO do not rescue NET formation, suggesting that MPO acts cell-autonomously. Finally, NET-dependent inhibition of Candida albicans growth is compromised in MPO-deficient neutrophils. The inability to form NETs may contribute in part to the host defense defects observed in completely MPO-deficient individuals.

scholarly journals Neutrophil extracellular traps impair regeneration

2020 ◽  
Author(s):  
Eric Wier ◽  
Mayumi Asada ◽  
Gaofeng Wang ◽  
Martin P. Alphonse ◽  
Ang Li ◽  
...  
Keyword(s):  
Hair Follicle ◽  
De Novo ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Extracellular Trap ◽  
Major Health ◽  
Net Production ◽  
Extracellular Traps ◽  
Single Cell Rna Sequencing ◽  
Neutrophil Depletion ◽  
Extracellular Trap

AbstractFibrosis is a major health burden across diseases and organs. To remedy, we study wound induced hair follicle regeneration (WIHN) as a model of non-fibrotic healing that instead recapitulates embryogenesis for de novo hair follicle morphogenesis after wounding. We have previously demonstrated that TLR3 promotes WIHN through binding dsRNA, but the source of which is still unclear. Here, we demonstrate that multiple distinct contexts of high WIHN all show a strong neutrophil signature, and given the likelihood of nuclear dsRNA release during the production of neutrophil extracellular trap (NETs), we hypothesized that neutrophils and NETs might promote WIHN. Consistent with this, in addition to the presence of neutrophils shortly after wounding, neutrophils remain within the wound after the barrier is reestablished, where they produce extracellular traps (NETs) that likely release spliceosomal U1 dsRNA. Contrary to our hypothesis, genetic models of neutrophil depletion show enhanced WIHN. Pad4 null mice that are defective in NET production also augment WIHN. Finally, using single-cell RNA sequencing, we identified a dramatic increase in neutrophil populations in the wound beds of low regenerating Tlr3-/- mice. Taken together, these results demonstrate that although neutrophils are stimulated by a common pro-regenerative cue, their presence and NETs can hinder regeneration.

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