Neutrophil extracellular traps in sterile inflammation: the story after dying?

Cui, Beibei; Tan, Chunyu; Schorn, Christine; Tang, Honghu; Liu, Yi; Zhao, Yi

doi:10.3109/08916934.2012.719952

Cited by 24 publications

(23 citation statements)

References 36 publications

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“…Studied primarily in models of infection, NETs are renowned for their ability to capture and disarm invading pathogens [3,33,34]. However, in recent years it has become increasingly apparent that NETs are also generated at sites of sterile inflammation [35,36].…”

Section: Microbicidal Functionmentioning

confidence: 99%

The impact of trauma on neutrophil function

Hazeldine

Hampson

Lord

2014

Injury

105

104

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A well described consequence of traumatic injury is immune dysregulation, where an initial increase in immune activity is followed by a period of immune depression, the latter leaving hospitalised trauma patients at an increased risk of nosocomial infections. Here, we discuss the emerging role of the neutrophil, the most abundant leucocyte in human circulation and the first line of defence against microbial challenge, in the initiation and propagation of the inflammatory response to trauma. We review the findings of the most recent studies to have investigated the impact of trauma on neutrophil function and discuss how alterations in neutrophil biology are being investigated as potential biomarkers by which to predict the outcome of hospitalised trauma patients. Furthermore, with trauma-induced changes in neutrophil biology linked to the development of such post-traumatic complications as multiple organ failure and acute respiratory distress syndrome, we highlight an area of research within the field of trauma immunology that is gaining considerable interest: the manipulation of neutrophil function as a means by which to potentially improve patient outcome.

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Section: Microbicidal Functionmentioning

confidence: 99%

The impact of trauma on neutrophil function

Hazeldine

Hampson

Lord

2014

Injury

105

104

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“…A role of NETs in tolerance-breaking and induction of autoimmunity is very probable, particularly in SLE (Bouts et al, 2012) and small-vessel vasculitis (Garcia-Romo et al, 2011; Cui et al, 2012; Sangaletti et al, 2012; Villanueva et al, 2012). Indeed, NET release exposes cytoplasmic, granular, and nuclear self antigens to the immune system.…”

Section: Introductionmentioning

confidence: 99%

An Improved Strategy to Recover Large Fragments of Functional Human Neutrophil Extracellular Traps

Barrientos¹,

Marin‐Esteban²,

Chaisemartin³

et al. 2013

Front. Immunol.

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Netosis is a recently described neutrophil function that leads to the release of neutrophil extracellular traps (NETs) in response to various stimuli. NETs are filaments of decondensed chromatin associated with granular proteins. In addition to their role against microorganisms, NETs have been implicated in autoimmunity, thrombosis, and tissue injury. Access to a standardized source of isolated NETs is needed to better analyze the roles of NETs. The aim of this study was to develop a procedure yielding soluble, well-characterized NET preparations from fresh human neutrophils. The calcium ionophore A23187 was chosen to induce netosis, and the restriction enzyme AluI was used to prepare large NET fragments. DNA and proteins were detected by electrophoresis and specific labeling. Some NET proteins [histone 3, lactoferrin (LF)] were quantified by western blotting, and double-stranded DNA (dsDNA) was quantified by immunofluorescence. Co-existence of dsDNA and neutrophil proteins confirmed the quality of the NET preparations. Their biological activity was checked by measuring elastase (ELA) activity and bacterial killing against various strains. Interindividual differences in histone 3, LF, ELA, and dsDNA relative contents were observed in isolated NETs. However, the reproducibility of NET preparation and characterization was validated, suggesting that this interindividual variability was rather related to donor variation than to technical bias. This standardized protocol is suitable for producing, isolating, and quantifying functional NETs that could serve as a tool for studying NET effects on immune cells and tissues.

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“…NET trap many types of microbes ex vivo and are found in various disease models in vivo; they are thought to kill microbes by exposing them to high local concentrations of antimicrobials [12] . Agents like bacteria, protozoa, fungi, and viruses as well as chemical and sterile inflammatory stimuli were shown to induce NETosis [10,13,14] . In the lungs, NET can be found in human allergic asthmatic airways [15] , and in mice upon influenza virus pneumonitis within the alveoli and airways, and in lesions of tissue injury [16] .…”

mentioning

confidence: 99%

Neutrophil Extracellular Traps Stimulate Proinflammatory Responses in Human Airway Epithelial Cells

Sabbione¹,

Keitelman²,

Iula³

et al. 2017

J Innate Immun

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Tissue injury leads to the release of uric acid (UA). At high local concentrations, UA can form monosodium urate crystals (MSU). MSU and UA stimulate neutrophils to release extracellular traps (NET). Here, we investigated whether these NET could be involved in the development of inflammation by stimulating cytokine release by airway epithelial cells. We found that NET significantly increased the secretion of CXCL8/IL-8 and IL-6 by alveolar and bronchial epithelial cells. These effects were not observed when NETosis was inhibited by Diphenyleneiodonium, elastase inhibitor, or Cl-amidine. Similar findings were made with NET induced by cigarette smoke extract, suggesting that NET proinflammatory capacity is independent of the inducing stimulus. Furthermore, NET affected neither the viability and morphology of epithelial cells nor the barrier integrity of polarized cells. The epithelial stimulatory capacity of NET was not affected by degradation of DNA with micrococcal nuclease, treatment with heparin, or inhibition of the elastase immobilized to DNA, but it was significantly reduced by pretreatment with an anti-HMGB-1 blocking antibody. Altogether, our findings indicate that NET exert direct proinflammatory effects on airway epithelial cells that might contribute in vivo to the further recruitment of neutrophils and the perpetuation of inflammation upon lung tissue damage.

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Neutrophil extracellular traps in sterile inflammation: the story after dying?

Cited by 24 publications

References 36 publications

The impact of trauma on neutrophil function

The impact of trauma on neutrophil function

An Improved Strategy to Recover Large Fragments of Functional Human Neutrophil Extracellular Traps

Neutrophil Extracellular Traps Stimulate Proinflammatory Responses in Human Airway Epithelial Cells

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