The Impact of Various Reactive Oxygen Species on the Formation of Neutrophil Extracellular Traps

Kirchner, Tina; Möller, Sonja; Klinger, Matthias; Solbach, Werner; Laskay, Tamás; Behnen, Martina

doi:10.1155/2012/849136

Cited by 188 publications

(184 citation statements)

References 36 publications

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“…Impressively, there has been a successful report of gene therapy, where an 8‐year‐old boy was treated with a retroviral vector containing a functional gp91 (PHOX subunit) gene, resulting in neutrophils regaining the ability to NETose and leading to a termination of an intractable Aspergillus nidans infection 51. Experimentally, inhibition of NADPHO or myeloperoxidase (MPO) effectively inhibited NETosis stimulated by PMA, whereas inhibition of mitochondrial respiration or superoxide dismutase did not 52. PHOX/NADPHO is itself activated by protein kinase C (PKC).…”

Section: Histone Processing and Active Release During Netosismentioning

confidence: 99%

Biology, role and therapeutic potential of circulating histones in acute inflammatory disorders

Szatmary

Huang

Criddle

et al. 2018

J Cellular Molecular Medi

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Histones are positively charged nuclear proteins that facilitate packaging of DNA into nucleosomes common to all eukaryotic cells. Upon cell injury or cell signalling processes, histones are released passively through cell necrosis or actively from immune cells as part of extracellular traps. Extracellular histones function as microbicidal proteins and are pro‐thrombotic, limiting spread of infection or isolating areas of injury to allow for immune cell infiltration, clearance of infection and initiation of tissue regeneration and repair. Histone toxicity, however, is not specific to microbes and contributes to tissue and end‐organ injury, which in cases of systemic inflammation may lead to organ failure and death. This review details the processes of histones release in acute inflammation, the mechanisms of histone‐related tissue toxicity and current and future strategies for therapy targeting histones in acute inflammatory diseases.

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Section: Histone Processing and Active Release During Netosismentioning

confidence: 99%

Biology, role and therapeutic potential of circulating histones in acute inflammatory disorders

Szatmary

Huang

Criddle

et al. 2018

J Cellular Molecular Medi

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“…The process involves a rapid externalization of chromatin (8). NET formation (NETosis) depends on reactive oxygen species (ROS) (9) and involves the receptor-interacting serine/threonineprotein kinase 3 (RIPK3) and the mixed lineage kinase domain-like (MLKL) of the necroptosis pathway (10) and various granular enzymes like myeloperoxidase (MPO) and neutrophil elastase (NE) (11). Importantly, neutrophil-driven inflammation is often selflimiting.…”

Section: Significancementioning

confidence: 99%

Nanoparticles size-dependently initiate self-limiting NETosis-driven inflammation

Muñoz

Bilyy

Biermann

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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118

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The critical size for strong interaction of hydrophobic particles with phospholipid bilayers has been predicted to be 10 nm. Because of the wide spreading of nonpolar nanoparticles (NPs) in the environment, we aimed to reveal the ability of living organisms to entrap NPs via formation of neutrophil extracellular traps (NETs). Upon interaction with various cell types and tissues, 10-to 40-nmsized NPs induce fast (<20 min) damage of plasma membranes and instability of the lysosomal compartment, leading to the immediate formation of NETs. In contrast, particles sized 100-1,000 nm behaved rather inertly. Resulting NET formation (NETosis) was accompanied by an inflammatory reaction intrinsically endowed with its own resolution, demonstrated in lungs and air pouches of mice. Persistence of small NPs in joints caused unremitting arthritis and bone remodeling. Small NPs coinjected with antigen exerted adjuvant-like activity. This report demonstrates a cellular mechanism that explains how small NPs activate the NETosis pathway and drive their entrapping and resolution of the initial inflammatory response.nanoparticles | size | neutrophils | NETosis | inflammation

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“…To study the kinetics of NET release of neutrophils, the non-cell-permeable DNA dye Sytox Green (Invitrogen) was used (2,4,12). Neutrophils (10 6 /ml) were incubated at 37˚C in iIC-coated Fluotrac 600 plates (Greiner Bio-One) in NET medium containing 5 mM Sytox Green.…”

Section: Detection Of Netsmentioning

confidence: 99%

“…NETs are composed of chromatin, histones, and antimicrobial proteins and contribute to pathogen containment (1). To release NETs, activated neutrophils undergo a form of cell death that is distinct from apoptosis and necrosis, the so-called NETosis (1,3), which is dependent on the formation of reactive oxygen species (ROS) and on NADPH oxidase (NOX) and myeloperoxidase (MPO) (3)(4)(5)(6)(7). In addition to ROS-dependent NETosis, few microorganisms and certain stimuli have been reported to induce NETs in an ROS-independent manner (8)(9)(10)(11).…”

mentioning

confidence: 99%

Immobilized Immune Complexes Induce Neutrophil Extracellular Trap Release by Human Neutrophil Granulocytes via FcγRIIIB and Mac-1

Behnen

Leschczyk

Möller

et al. 2014

The Journal of Immunology

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213

191

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Canonical neutrophil antimicrobial effector mechanisms, such as degranulation, production of reactive oxygen species, and release of neutrophil extracellular traps (NETs), can result in severe pathology. Activation of neutrophils through immune complexes (ICs) plays a central role in the pathogenesis of many autoimmune inflammatory diseases. In this study, we report that immobilized ICs (iICs), which are hallmarks of several autoimmune diseases, induce the release of NETs from primary human neutrophils. The iIC-induced NET formation was found to require production of reactive oxygen species by NADPH oxidase and myeloperoxidase and to be mediated by FcγRIIIb. Blocking of the β2 integrin macrophage-1 Ag but not lymphocyte function–associated Ag-1 abolished iIC-induced NET formation. This suggests that FcγRIIIb signals in association with macrophage-1 Ag. As intracellular signaling pathways involved in iIC-induced NET formation we identified the tyrosine kinase Src/Syk pathway, which downstream regulates the PI3K/Akt, p38 MAPK, and ERK1/2 pathways. To our knowledge, the present study shows for the first time that iICs induce NET formation. Thus, we conclude that NETs contribute to pathology in autoimmune inflammatory disorders associated with surface-bound ICs.

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The Impact of Various Reactive Oxygen Species on the Formation of Neutrophil Extracellular Traps

Cited by 188 publications

References 36 publications

Biology, role and therapeutic potential of circulating histones in acute inflammatory disorders

Biology, role and therapeutic potential of circulating histones in acute inflammatory disorders

Nanoparticles size-dependently initiate self-limiting NETosis-driven inflammation

Immobilized Immune Complexes Induce Neutrophil Extracellular Trap Release by Human Neutrophil Granulocytes via FcγRIIIB and Mac-1

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