scholarly journals Alterations in neutrophil extracellular traps is associated with the degree of decompensation of liver cirrhosis

2016 ◽  
Vol 10 (05) ◽  
pp. 512-517 ◽  
Author(s):  
Juan M Agraz-Cibrian ◽  
Jorge E Segura-Ortega ◽  
Vidal Delgado-Rizo ◽  
Mary Fafutis-Morris
Keyword(s):  
Liver Cirrhosis ◽  
Bacterial Infections ◽  
Causes Of Death ◽  
Serum Levels ◽  
Study Groups ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Activation ◽  
Neutrophil Extracellular Trap ◽  
Activation Markers ◽  
Extracellular Traps

Introduction: Liver cirrhosis (LC) constitutes one of the main 10 causes of death worldwide. LC has a characteristic asymptomatic compensated phase followed by a progressive decompensated phase, in which diverse complications are presented. LC patients are highly prone to bacterial infections. The neutrophils in these patients present defects in the production of oxygen radicals, which are essential for bacteria elimination as in the activation of neutrophil extracellular traps (NETs). The main objective of this work was to determine the NETs and neutrophil activation markers in LC patients. Methodology: Neutrophil purification was done with Ficoll Histopaque from a sample of the peripheral blood of patients with compensated and decompensated LC. Neutrophils were activated with Phorbol 12-myristate 13-acetate to evaluate the release of NETs by means of fluorescence microscopy and fluorometry, while expression of activation markers (CD69, CD80, perforin, and CAP-18) was evaluated by flow cytometry. Results: A significant decrease in the release capability of NETs was observed as the level of LC in the patient increased. When comparing serum levels in inflammatory cytokines among the different study groups, significant differences were observed. No significant differences were detected on neutrophil activation markers; nevertheless, there was a correlation between diminution of CD69 and CD80 expression in decompensated patients. Conclusions: We demonstrated that LC patients with neutrophil extracellular trap release deficiencies could have an increased rate of complications.

scholarly journals Prognostic value of circulating markers of neutrophil activation, neutrophil extracellular traps, coagulation and fibrinolysis in patients with terminal cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Axel Rosell ◽  
Katherina Aguilera ◽  
Yohei Hisada ◽  
Clare Schmedes ◽  
Nigel Mackman ◽  
...  
Keyword(s):  
Advanced Cancer ◽  
Prognostic Value ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Activation ◽  
Terminal Cancer ◽  
Extracellular Traps ◽  
Terminal Cancer Patients ◽  
Future Care ◽  
Circulating Markers ◽  
Coagulation And Fibrinolysis

AbstractPredicting survival accurately in patients with advanced cancer is important in guiding interventions and planning future care. Objective tools are therefore needed. Blood biomarkers are appealing due to their rapid measurement and objective nature. Thrombosis is a common complication in cancer. Recent data indicate that tumor-induced neutrophil extracellular traps (NETs) are pro-thrombotic. We therefore performed a comprehensive investigation of circulating markers of neutrophil activation, NET formation, coagulation and fibrinolysis in 106 patients with terminal cancer. We found that neutrophil activation and NET markers were prognostic in terminal cancer patients. Interestingly, markers of coagulation and fibrinolysis did not have a prognostic value in this patient group, and there were weak or no correlations between these markers and markers of neutrophil activation and NETs. This suggest that NETs are linked to a poor prognosis through pathways independent of coagulation. Additional studies are needed to determine the utility of circulating neutrophil activation and NET markers, alone or in concert with established clinical parameters, as objective and reliable prognostic tools in advanced cancer.

scholarly journals S100A9 in adult asthmatic patients: a biomarker for neutrophilic asthma

2021 ◽  
Author(s):  
Quang Luu Quoc ◽  
Youngwoo Choi ◽  
Tra Cao Thi Bich ◽  
Eun-Mi Yang ◽  
Yoo Seob Shin ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Macrophage Polarization ◽  
Serum Levels ◽  
Lavage Fluid ◽  
Airway Epithelial Cells ◽  
Neutrophil Activation ◽  
Neutrophil Extracellular Trap ◽  
Airway Epithelial ◽  
Asthmatic Patients ◽  
M1 Macrophage

AbstractThe biomarkers and therapeutic targets of neutrophilic asthma (NA) are poorly understood. Although S100 calcium-binding protein A9 (S100A9) has been shown to correlate with neutrophil activation, its role in asthma pathogenesis has not been clarified. This study investigated the mechanism by which S100A9 is involved in neutrophil activation, neutrophil extracellular trap (NET)-induced airway inflammation, and macrophage polarization in NA. The S100A9 levels (by ELISA) in sera/culture supernatant of peripheral blood neutrophils (PBNs) and M0 macrophages from asthmatic patients were measured and compared to those of healthy controls (HCs). The function of S100A9 was evaluated using airway epithelial cells (AECs) and PBNs/M0 macrophages from asthmatic patients, as well as a mouse asthma model. The serum levels of S100A9 were higher in NA patients than in non-NA patients, and there was a positive correlation between serum S100A9 levels and sputum neutrophil counts (r = 0.340, P = 0.005). Asthmatic patients with higher S100A9 levels had lower PC20 methacholine values and a higher prevalence of severe asthma (SA) (P < .050). PBNs/M0 macrophages from SA released more S100A9 than those from non-SA patients. PBNs from asthmatic patients induced S100A9 production by AECs, which further activated AECs via the extracellular signal-regulated kinase (ERK) pathway, stimulated NET formation, and induced M1 macrophage polarization. Higher S100A9 levels in sera, bronchoalveolar lavage fluid, and lung tissues were observed in the mouse model of NA but not in the other mouse models. These results suggest that S100A9 is a potential serum biomarker and therapeutic target for NA.

Neutrophil Extracellular Traps May Contribute to the Pathogenesis in Adult-onset Still Disease

2019 ◽  
Vol 46 (12) ◽  
pp. 1560-1569 ◽  
Author(s):  
Mi-Hyun Ahn ◽  
Jae Ho Han ◽  
Young-Jun Chwae ◽  
Ju-Yang Jung ◽  
Chang-Hee Suh ◽  
...  
Keyword(s):  
Immunohistochemical Analysis ◽  
Serum Levels ◽  
Neutrophil Extracellular Traps ◽  
Polymorphonuclear Neutrophils ◽  
Adult Onset ◽  
Cell Free Dna ◽  
Extracellular Traps ◽  
Free Dna ◽  
Still Disease

Objective.Release of neutrophil extracellular traps (NET) has been described as an effector mechanism of polymorphonuclear neutrophils in several inflammatory diseases. Thus, this study was performed to evaluate the role of NET in the pathogenesis of adult-onset Still disease (AOSD).Methods.We determined the serum levels of NET molecules and investigated their associations with clinical disease activities in patients with AOSD. Further, we analyzed the differences in the NETosis response in AOSD patients compared to healthy controls (HC). To explore the in vivo involvement of NET in AOSD, we performed immunohistochemical analysis of skin and lymph node (LN) biopsies for proteins related to NET in patients with active AOSD.Results.Serum levels of cell-free DNA, myeloperoxidase (MPO)-DNA complex, and α-defensin were significantly increased in patients with AOSD compared to HC. Serum levels of the NET molecules, cell-free DNA, MPO-DNA, and α-defensin were correlated with several disease activity markers for AOSD. In followup of patients with AOSD after treatment with corticosteroid, the levels of cell-free DNA and α-defensin decreased significantly. On immunohistochemistry, neutrophil elastase–positive and MPO-positive inflammatory cells were detected in skin and LN of patients with AOSD, and were expressed in fiber form in the lesions. The serum from patients with active AOSD induced NETosis in neutrophils from HC. NET molecules induced interleukin 1β production in monocytes, representing a novel mechanism in the pathogenesis of AOSD.Conclusion.The findings presented here suggest that NET may contribute to the inflammatory response and pathogenesis in AOSD.

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 Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19

2020 ◽  
Author(s):  
Corleone Delaveris ◽  
Aaron Wilk ◽  
Nicholas Riley ◽  
Jessica Stark ◽  
Samuel Yang ◽  
...  
Keyword(s):  
Immune Response ◽  
Therapeutic Strategy ◽  
Neutrophil Extracellular Traps ◽  
Neutrophil Activation ◽  
Signaling Cascade ◽  
Peripheral Inflammation ◽  
Pulmonary Tissue ◽  
Extracellular Traps ◽  
Cell Death Pathway ◽  
Key Factor

Severe cases of coronavirus disease 2019 (COVID-19), caused by infection with SARS-Cov-2, are characterized by a hyperinflammatory immune response that leads to numerous complications. Production of proinflammatory neutrophil extracellular traps (NETs) has been suggested to be a key factor in inducing a hyperinflammatory signaling cascade, allegedly causing both pulmonary tissue damage and peripheral inflammation. Accordingly, therapeutic blockage of neutrophil activation and NETosis, the cell death pathway accompanying NET formation, could limit respiratory damage and death from severe COVID-19. Here, we demonstrate that synthetic glycopolymers that activate the neutrophil checkpoint receptor Siglec-9 suppress NETosis induced by agonists of viral toll-like receptors (TLRs) and plasma from patients with severe COVID-19. Thus, Siglec-9 agonism is a promising therapeutic strategy to curb neutrophilic hyperinflammation in COVID-19.<br>

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.

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