scholarly journals Neutrophil Extracellular Traps: As Antimicrobial Peptides

2019 ◽  
pp. 1-9 ◽  
Author(s):  
Quratul Ann
Keyword(s):  
Blood Circulation ◽  
Immune Reaction ◽  
Inflammatory Diseases ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Neutrophil Extracellular Trap ◽  
Oxygen Species ◽  
Extracellular Traps ◽  
Response System ◽  
Infection And Inflammation

Neutrophils are an integral part of innate immune response system, abundantly present in blood circulation. They are the primary responders to the injury or intruding pathogens in human body. Neutrophils engulf infectious microorganisms by the process of phagocytosis, which usually initiates the production of reactive oxygen species and adhere the neutrophilic antimicrobial granules with vacuoles containing pathogens. Upon activation, neutrophils also render signals for stimulation and maturation of macrophages and dendritic cells. They release neutrophil extracellular traps for the suppression of infection and inflammation along with other antimicrobial molecules. The antimicrobials that are present in neutrophil extracellular traps not only eradicate microbes but also moderately contribute to the pathogenesis of various diseases such as destruction of tissue observed in periodontitis. Genetic shortcomings in neutrophils with respect to their chemotaxis, migration and phagocytosis become evident as severe forms of periodontitis, thus highlighting their role in innate immunity. Therefore, the present review is undertaken to highlight the importance of production and release of neutrophil extracellular trap in the regulation of immune reaction and its role in periodontal disease. A comprehensive database search was performed to gather all the relevant data related to the action of neutrophil and neutrophil extracellular traps in various inflammatory diseases with special emphasis on periodontitis.

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 A Review of the Neutrophil Extracellular Traps (NETs) from Cow, Sheep and Goat Models

2021 ◽  
Vol 22 (15) ◽  
pp. 8046
Author(s):  
Mulumebet Worku ◽  
Djaafar Rehrah ◽  
Hamid D. Ismail ◽  
Emmanuel Asiamah ◽  
Sarah Adjei-Fremah
Keyword(s):  
One Health ◽  
Inflammatory Diseases ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Response Mechanism ◽  
Global Food Security ◽  
Extracellular Traps ◽  
Definition Of ◽  
Global Food ◽  
Insight Into

This review provides insight into the importance of understanding NETosis in cows, sheep, and goats in light of the importance to their health, welfare and use as animal models. Neutrophils are essential to innate immunity, pathogen infection, and inflammatory diseases. The relevance of NETosis as a conserved innate immune response mechanism and the translational implications for public health are presented. Increased understanding of NETosis in ruminants will contribute to the prediction of pathologies and design of strategic interventions targeting NETs. This will help to control pathogens such as coronaviruses and inflammatory diseases such as mastitis that impact all mammals, including humans. Definition of unique attributes of NETosis in ruminants, in comparison to what has been observed in humans, has significant translational implications for one health and global food security, and thus warrants further study.

scholarly journals Neutrophil Extracellular Traps as Innate Immune Reaction against the Emerging Apicomplexan Parasite Besnoitia besnoiti

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e91415 ◽  
Author(s):  
Tamara Muñoz Caro ◽  
Carlos Hermosilla ◽  
Liliana M. R. Silva ◽  
Helder Cortes ◽  
Anja Taubert
Keyword(s):  
Immune Reaction ◽  
Neutrophil Extracellular Traps ◽  
Apicomplexan Parasite ◽  
Innate Immune ◽  
Besnoitia Besnoiti ◽  
Extracellular Traps

scholarly journals Neutrophil Extracellular Traps Affecting Cardiovascular Health in Infectious and Inflammatory Diseases

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1689
Author(s):  
Manovriti Thakur ◽  
Bryce Evans ◽  
Marc Schindewolf ◽  
Iris Baumgartner ◽  
Yvonne Döring
Keyword(s):  
Cardiovascular Health ◽  
Viral Infections ◽  
Inflammatory Diseases ◽  
Vascular Inflammation ◽  
Neutrophil Extracellular Traps ◽  
Immune Defense ◽  
Future Research ◽  
Extracellular Traps ◽  
Infection And Inflammation

Neutrophil extracellular traps (NETs) are web-like structures of decondensed extracellular chromatin fibers and neutrophil granule proteins released by neutrophils. NETs participate in host immune defense by entrapping pathogens. They are pro-inflammatory in function, and they act as an initiator of vascular coagulopathies by providing a platform for the attachment of various coagulatory proteins. NETs are diverse in their ability to alter physiological and pathological processes including infection and inflammation. In this review, we will summarize recent findings on the role of NETs in bacterial/viral infections associated with vascular inflammation, thrombosis, atherosclerosis and autoimmune disorders. Understanding the complex role of NETs in bridging infection and chronic inflammation as well as discussing important questions related to their contribution to pathologies outlined above may pave the way for future research on therapeutic targeting of NETs applicable to specific infections and inflammatory disorders.

scholarly journals Neutrophil Extracellular Traps in the Establishment and Progression of Renal Diseases

Medicina ◽  
2019 ◽  
Vol 55 (8) ◽  
pp. 431 ◽  
Author(s):  
Hector Salazar-Gonzalez ◽  
Alexa Zepeda-Hernandez ◽  
Zesergio Melo ◽  
Diego Eduardo Saavedra-Mayorga ◽  
Raquel Echavarria
Keyword(s):  
Inflammatory Diseases ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Renal Diseases ◽  
Glomerular Injury ◽  
Kidney Fibrosis ◽  
Extracellular Traps ◽  
Autoimmune Processes ◽  
Pro Inflammatory Cytokines

Uncontrolled inflammatory and immune responses are often involved in the development of acute and chronic forms of renal injury. Neutrophils are innate immune cells recruited early to sites of inflammation, where they produce pro-inflammatory cytokines and release mesh-like structures comprised of DNA and granular proteins known as neutrophil extracellular traps (NETs). NETs are potentially toxic, contribute to glomerular injury, activate autoimmune processes, induce vascular damage, and promote kidney fibrosis. Evidence from multiple studies suggests that an imbalance between production and clearance of NETs is detrimental for renal health. Hence strategies aimed at modulating NET-associated processes could have a therapeutic impact on a myriad of inflammatory diseases that target the kidney. Here, we summarize the role of NETs in the pathogenesis of renal diseases and their mechanisms of tissue damage.

scholarly journals Role of Neutrophils on the Ocular Surface

2021 ◽  
Vol 22 (19) ◽  
pp. 10386
Author(s):  
Yongseok Mun ◽  
Jin Sun Hwang ◽  
Young Joo Shin
Keyword(s):  
Ocular Surface ◽  
Innate Immune System ◽  
Neutrophil Infiltration ◽  
Neutrophil Extracellular Traps ◽  
Therapeutic Agents ◽  
Innate Immune ◽  
Neutrophil Extracellular Trap ◽  
Extracellular Traps ◽  
Ocular Surface Diseases

The ocular surface is a gateway that contacts the outside and receives stimulation from the outside. The corneal innate immune system is composed of many types of cells, including epithelial cells, fibroblasts, natural killer cells, macrophages, neutrophils, dendritic cells, mast cells, basophils, eosinophils, mucin, and lysozyme. Neutrophil infiltration and degranulation occur on the ocular surface. Degranulation, neutrophil extracellular traps formation, called NETosis, and autophagy in neutrophils are involved in the pathogenesis of ocular surface diseases. It is necessary to understand the role of neutrophils on the ocular surface. Furthermore, there is a need for research on therapeutic agents targeting neutrophils and neutrophil extracellular trap formation for ocular surface diseases.

scholarly journals Start a fire, kill the bug: The role of platelets in inflammation and infection

2018 ◽  
Vol 24 (6) ◽  
pp. 335-348 ◽  
Author(s):  
Carsten Deppermann ◽  
Paul Kubes
Keyword(s):  
Immune Cells ◽  
Innate Immune System ◽  
Current Knowledge ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Oxygen Species ◽  
Vascular Integrity ◽  
Surface Receptors ◽  
Extracellular Traps

Platelets are the main players in thrombosis and hemostasis; however they also play important roles during inflammation and infection. Through their surface receptors, platelets can directly interact with pathogens and immune cells. Platelets form complexes with neutrophils to modulate their capacities to produce reactive oxygen species or form neutrophil extracellular traps. Furthermore, they release microbicidal factors and cytokines that kill pathogens and influence the immune response, respectively. Platelets also maintain the vascular integrity during inflammation by a mechanism that is different from classical platelet activation. In this review we summarize the current knowledge about how platelets interact with the innate immune system during inflammation and infection and highlight recent advances in the field.

scholarly journals S100A8/A9 Is a Marker for the Release of Neutrophil Extracellular Traps and Induces Neutrophil Activation

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 236
Author(s):  
Evelien G. G. Sprenkeler ◽  
Judith Zandstra ◽  
Nadine D. van Kleef ◽  
Ines Goetschalckx ◽  
Bibian Verstegen ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Activation ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Intracellular Protein ◽  
Cytoplasmic Fraction ◽  
Extracellular Traps ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Neutrophils are the most abundant innate immune cells in the circulation and they are the first cells recruited to sites of infection or inflammation. Almost half of the intracellular protein content in neutrophils consists of S100A8 and S100A9, though there has been controversy about their actual localization. Once released extracellularly, these proteins are thought to act as damage-associated molecular patterns (DAMPs), though their mechanism of action is not well understood. These S100 proteins mainly form heterodimers (S100A8/A9, also known as calprotectin) and this heterocomplex is recognized as a useful biomarker for several inflammatory diseases. We observed that S100A8/A9 is highly present in the cytoplasmic fraction of neutrophils and is not part of the granule content. Furthermore, we found that S100A8/A9 was not released in parallel with granular content but upon the formation of neutrophil extracellular traps (NETs). Accordingly, neutrophils of patients with chronic granulomatous disease, who are deficient in phorbol 12-myristate 13-acetate (PMA)-induced NETosis, did not release S100A8/A9 upon PMA stimulation. Moreover, we purified S100A8/A9 from the cytoplasmic fraction of neutrophils and found that S100A8/A9 could induce neutrophil activation, including adhesion and CD11b upregulation, indicating that this DAMP might amplify neutrophil activation.

scholarly journals Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps

2010 ◽  
Vol 191 (3) ◽  
pp. 677-691 ◽  
Author(s):  
Venizelos Papayannopoulos ◽  
Kathleen D. Metzler ◽  
Abdul Hakkim ◽  
Arturo Zychlinsky
Keyword(s):  
Immune Deficiency ◽  
Neutrophil Elastase ◽  
Serine Proteases ◽  
Neutrophil Extracellular Traps ◽  
Oxygen Species ◽  
Chromatin Decondensation ◽  
Unknown Mechanism ◽  
Extracellular Traps ◽  
Decondensed Chromatin ◽  
Chromatin Density

Neutrophils release decondensed chromatin termed neutrophil extracellular traps (NETs) to trap and kill pathogens extracellularly. Reactive oxygen species are required to initiate NET formation but the downstream molecular mechanism is unknown. We show that upon activation, neutrophil elastase (NE) escapes from azurophilic granules and translocates to the nucleus, where it partially degrades specific histones, promoting chromatin decondensation. Subsequently, myeloperoxidase synergizes with NE in driving chromatin decondensation independent of its enzymatic activity. Accordingly, NE knockout mice do not form NETs in a pulmonary model of Klebsiella pneumoniae infection, which suggests that this defect may contribute to the immune deficiency of these mice. This mechanism provides for a novel function for serine proteases and highly charged granular proteins in the regulation of chromatin density, and reveals that the oxidative burst induces a selective release of granular proteins into the cytoplasm through an unknown mechanism.

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