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Neutrophil Extracellular Traps in Immunity and Disease

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Neutrophil Extracellular Traps in Immunity and Disease REVIEWS Neutrophil extracellular traps in immunity and disease Venizelos Papayannopoulos Abstract | Neutrophils are innate immune phagocytes that have a central role in immune defence. Our understanding of the role of neutrophils in pathogen clearance, immune regulation and disease pathology has advanced dramatically in recent years. Web-like chromatin structures known as neutrophil extracellular traps (NETs) have been at the forefront of this renewed interest in neutrophil biology. The identification of molecules that modulate the release of NETs has helped to refine our view of the role of NETs in immune protection, inflammatory and autoimmune diseases and cancer. Here, I discuss the key findings and concepts that have thus far shaped the field of NET biology. Neutrophil elastase Neutrophils are the most abundant innate immune Next, the nuclear envelope disassembles, and nuclear (NE). A neutrophil-specific effector cells of the human immune system. They chromatin decondenses into the cytoplasm of intact antimicrobial serine protease are armed with broadly effective antimicrobials that are cells, mixing with cytoplasmic and granule components10 stored in azurophilic granules. stored predominately in specialized granules. Given that (FIG. 1). The plasma membrane then permeabilizes, and this neutrophil arsenal can also damage host tissues, its NETs expand into the extracellular space 3–8 hours after Myeloperoxidase (MPO). A haem-containing deployment is tightly regulated through three major neutrophil activation. An alternative mechanism termed enzyme that reacts with strategies: phagocytosis, degranulation and the release non-lytic NETosis leads to the rapid release of NETs hydrogen peroxide to generate of neutrophil extracellular traps (NETs). NETs are large, within minutes of exposure to Staphylococcus aureus hypochlorite and other halide extracellular, web-like structures composed of cytosolic via the secretion of chromatin and granule contents12,13 oxidants. and granule proteins that are assembled on a scaffold of and in the absence of cell death. This phenomenon decondensed chromatin1. Although the majority of DNA has been observed by intravital microscopy in a small in NETs originates from the nucleus, these structures fraction of neutrophils during systemic S. aureus infec- also contain mitochondrial DNA2. NETs trap, neutralize tion and generates NETs and anucleated cytoplasts that and kill bacteria1, fungi3, viruses4 and parasites5 and are crawl and phagocytose bacteria13. This multitasking non- thought to prevent bacterial and fungal dissemination6,7. lytic rapid response is mounted by the first neutrophils to However, if dysregulated, NETs can contribute to the arrive at sites of infection. pathogenesis of immune-related diseases. The mechanisms that clear NETs are less well under- Initially, 24 proteins were identified in NETs formed stood. During infection, NETs persist for several days7 by stimulation of neutrophils with phorbol 12-myristate and are thought to be dismantled by the secreted plasma 13-acetate (PMA), a molecule that activates protein nuclease DNase I (REF. 14). Injection of this enzyme dur- kinase C (PKC) and triggers the production of reactive ing S. aureus infection leads to rapid degradation of NET- oxygen species (ROS). Among these proteins were his- associated DNA15, but the dynamics of NET clearance by tones, the serine protease neutrophil elastase (NE; also endogenous enzymes are unknown. Strikingly, NET pro- known as ELANE), myeloperoxidase (MPO), calprotectin, teins persist long after DNA degradation15, suggesting that cathelicidins, defensins and actin8. Subsequent studies they are cleared via additional mechanisms. These mecha- have extended this list, suggesting that the composition of nisms might involve macrophage scavenging, as DNase I NETs varies depending on the stimulus. For example, dif- facilitates the ingestion of NETs by macrophages in vitro16. ferent Pseudomonas aeruginosa mucoid and non-mucoid Here, I provide an overview of the mechanisms that strains induce the formation of NETs containing 33 com- regulate NET formation and clearance and describe mon proteins and up to 50 variable proteins9. Whether recent advances in our understanding of how NETs pro- The Francis Crick Institute, 1 Midland Road, London and how differences in NET composition impact NET tect against infection and cause pathology associated with NW1 1AT, UK. function remains to be investigated. several diseases. These topics are organized in a concep- [email protected] NET release occurs primarily through a cell death tual manner according to the immunological function 10 doi:10.1038/nri.2017.105 process termed NETosis . To initiate this process, of NETs. I pay attention to key findings, highlight open Published online 9 Oct 2017 neutro phils arrest their actin dynamics and depolarize11. questions and discuss the controversies in the field. 134 | FEBRUARY 2018 | VOLUME 18 www.nature.com/nri ©2018 Mac millan Publishers Li mited, part of Spri nger Nature. All ri ghts reserved. ©2018 Mac millan Publishers Li mited, part of Spri nger Nature. All ri ghts reserved. REVIEWS Granule Nucleus NET NETosis (slow cell death) • Nuclear • Cellular delobulation depolarization • Plasma membrane • Disassembly of • Chromatin rupture nuclear envelope decondensation • Release of NETs Extracellular Neutrophil assembly of NET NET Non-lytic NETosis (rapid release from live cells) Phagocytic cytoplast • Degranulation • Expulsion of nuclear chromatin Figure 1 | NET formation pathways. Neutrophil extracellular traps (NETs) form via two pathways. The first is a cell death pathway termed NETosis that begins with nuclear delobulation and the disassemblyNature of the Reviewsnuclear envelope | Immunology and continues with loss of cellular polarization, chromatin decondensation and plasma membrane rupture. The second is a non-lytic form of NETosis that can occur independently of cell death and involves the secreted expulsion of nuclear chromatin that is accompanied by the release of granule proteins through degranulation. These components assemble extracellularly and leave behind active anucleated cytoplasts that continue to ingest microorganisms. NADPH oxidase Mechanisms of NET formation supported by studies of neutrophils from patients with A membrane-associated chronic granulomatous disease 10 complex of proteins that From ROS to chromatin decondensation. Two enzymes (CGD) and with com- 18 transfer electrons from NADPH in the ROS pathway have critical roles in NETosis. plete MPO deficiency , as well as by studies using to molecular oxygen to ROS generated by NADPH oxidase stimulate MPO to NE-deficient mice or NE inhibitors in mouse models generate the oxygen radical trigger the activation and translocation of NE from of sepsis, cancer and pulmonary infection7,15,17,21. NET superoxide. azurophilic granules to the nucleus, where NE proteo- release is also abrogated in NADPH oxidase-deficient Azurophilic granules lytically processes histones to disrupt chromatin pack- mice during pulmonary fungal infection, which stim- A subset of neutrophil granules aging17. Subsequently, MPO binds chromatin and ulates robust NET release22. Similarly, NETosis is defec- that contain antimicrobials synergizes with NE in decondensing chromatin inde- tive in neutrophils from patients with Papillon–Lefèvre such as myeloperoxidase and pendently of its enzymatic activity17 (FIG. 2). NADPH syndrome caused by mutations in the cysteine pro- neutrophil elastase. Within the granule membranes, a complex oxidase activity can be redundant in response to tease cathepsin C (CTSC), which processes NE into its 23,24 of eight antimicrobial proteins some stimuli, such as immune complexes in which mature form . Mice lacking CTSC fail to form NETs forms the azurosome. mito chondrial ROS are sufficient to drive NETosis2. upon pulmonary Sendai virus infection25 and in aortic NE release from azurophilic granules does not aneurism models26. Moreover, isolated CTSC-deficient Chronic granulomatous disease require membrane rupture or fusion. In resting neutro- neutrophils exhibit defects in NETosis, although the (CGD). An inherited X-linked phils, a fraction of MPO is bound to NE as part of a impairment is less striking than that observed after immune deficiency caused by complex called the azurosome, which spans granule pharmacological NE inhibition. genetic mutations that disrupt membranes11. Hydrogen peroxide selectively releases One study challenged the requirement of NE in the activity of NADPH oxidase. NE into the cytosol in an MPO-dependent manner NETosis 27 on the basis of experiments with PMA-induced It is associated with (FIG. 2) hyperinflammation and . It is important to clarify that inhibition of the mouse neutrophils that yielded low levels of NETs. By increased susceptibility to enzymatic activity of MPO does not block but only contrast, NE deficiency and inhibitors attenuated NETosis bacterial and fungal infections. delays NETosis18, potentially owing to the role of MPO upon stimulation with the Ca2+ ionophore ionomycin, in activating the proteolytic activity of NE against which induced a robust response27. In the same study, Thrombosis thrombosis Formation of a blood clot large protein substrates. This oxidative activation NE deficiency did not reduce NET-mediated 27 28 (thrombus) in blood vessels, is important because NE binds to F-actin filaments in vivo , but this result contradicts prior literature . resulting in partial or complete in the cytoplasm and must
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