Nitric oxide donors release extracellular traps from human neutrophils by augmenting free radical generation

Patel, Satyananda; Kumar, Sachin; Jyoti, Anupam; Srinag, Bangalore Suresh; Keshari, Ravi S.; Saluja, Rohit; Verma, Anupam; Mitra, Kalyan; Barthwal, Manoj Kumar; Krishnamurthy, Hanumanthappa; Bajpai, V.K.; Dikshit, Madhu

doi:10.1016/j.niox.2010.01.001

Cited by 138 publications

(125 citation statements)

References 51 publications

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“…Previous studies have found that TLR4 engagement as well as production of ROS by NADPH oxidase can induce NET formation (10,13,34). Exposure of neutrophils to PMA resulted in activation of NADPH oxidase and extensive NET formation (Fig.…”

Section: Hmgb1 Induces the Formation Of Neutrophil Extracellular Trapsmentioning

confidence: 76%

“…Although the role that myeloperoxidase plays in DNA release has not been delineated, recent studies suggest that myeloperoxidase embedded in NETs may facilitate microbial killing (33). Previous studies have shown that activation of NADPH oxidase and production of ROS can trigger NET formation (6,34,38). Although exposure of neutrophils to the flavoprotein inhibitor DPI diminished NADPH oxidase-mediated NET formation, DPI had no effect on HMGB1-dependent release of DNA into the extracellular space.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to DNA, NETs contain additional proteins that may facilitate microbial eradication, including histones, elastase, and myeloperoxidase (26,32,33,46). NETs are formed in response to proinflammatory stimuli, including LPS, IL-8, and TNF-␣, as well as through enhanced reactive oxygen species (ROS) generation by NADPH oxidase (8,10,33,34,36).…”

mentioning

confidence: 99%

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HMGB1 promotes neutrophil extracellular trap formation through interactions with Toll-like receptor 4

Tadié

Bae

Jiang³

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

285

205

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Although neutrophil extracellular traps (NETs) form to prevent dissemination of pathogenic microorganisms, excessive release of DNA and DNA-associated proteins can also perpetuate sterile inflammation. In this study, we found that the danger-associated molecular pattern protein high-mobility group box 1 (HMGB1) can induce NET formation. NET formation was found after exposure of wild-type and receptor for advanced glycation end products-deficient neutrophil to HMGB1, whereas deficiency of Toll-like receptor (TLR)4 diminished the ability of neutrophils to produce NETs. Incubation of neutrophils with HMGB1 significantly increased the amount of DNA and histone 3 released as well as intracellular histone 3 citrullination, a signaling event that precedes chromatin decondensation. In vivo, neutrophils isolated from bronchoalveolar lavages of mice exposed to LPS and HMGB1 showed consistently greater ability to produce NETs compared with pulmonary neutrophils from mice that received LPS alone. In contrast, mice treated with LPS and neutralizing antibody to HMGB1 had decreased amounts of the inflammatory cytokines TNF-α and macrophage inflammatory protein 2, as well as of free DNA and histone 3 in bronchoalveolar lavage fluids. Airway neutrophils from LPS-exposed mice that had been treated with anti-HMGB1 antibodies showed decreased citrullination of histone 3. These results demonstrate that interactions between HMGB1 and TLR4 enhance the formation of NETs and provide a novel mechanism through which HMGB1 may contribute to the severity of neutrophil-associated inflammatory conditions.

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Section: Hmgb1 Induces the Formation Of Neutrophil Extracellular Trapsmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

HMGB1 promotes neutrophil extracellular trap formation through interactions with Toll-like receptor 4

Tadié

Bae

Jiang³

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

285

205

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“…In spite of the early, very convincing work showing that PMA could not induce NETs in the absence of oxidants, and that humans with NADPH-oxidase deficiency could not make NETs, [9][10][11][12][13] there is now growing evidence to suggest that some stimuli induce NETs independently of NADPH oxidase. Indeed, Staphylococcus aureus appears to induce NETs in a rapid fashion before any intracellular oxidative stress could be detected.…”

Section: Suicidal Netosismentioning

confidence: 99%

NETosis: how vital is it?

Yipp¹,

Kubes

2013

Blood

806

793

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In this review, we examine the evidence that neutrophil extracellular traps (NETs) play a critical role in innate immunity. We summarize how NETs are formed in response to various stimuli and provide evidence that NETosis is not universally a cell death pathway. Here we describe at least 2 different mechanisms by which NETs are formed, including a suicide lytic NETosis and a live cell or vital NETosis. We also evaluate the evidence for NETs in catching and killing pathogens. Finally, we examine how infections are related to the development of autoimmune and vasculitic diseases through unintended but detrimental bystander damage resulting from NET release.

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“…Keshari et al 70 have correlated the augmented level of TNF-, IL-1 and IL-8 with increased PMN ROS generation in SIRS patients, which results in neutrophil extracellular traps (NETs) formation. Role of NO in NETs release through free-radical generation involving NOX and MPO has been reported 71 . Another ROS-producing moiety, XO has been shown to be upregulated under various inflammatory conditions like airway inflammatory disorders, ischaemia reperfusion injury, atherosclerosis, diabetes and autoimmune disorders such as rheumatoid arthritis 72 .…”

Section: Free Radicals In Inflammationmentioning

confidence: 99%

Ageing:Consequences of Excessive Free Radicals and Inflammation

Jyoti

Dhas

2016

Current Science

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Free radicals, including reactive oxygen species (ROS) as well as reactive nitrogen species (RNS), and inflammation increase with advancing age. Evidence suggests that oxidative stress and inflammation both lead to impaired vascular function. There is also evidence to suggest that inflammation may cause an increase in radical production leading to enhanced oxidative/nitrosative stress. In addition, higher concentration of free radicals also modulates inflammation by increasing the expression of inflammatory proteins, including cytokines. Although ROS/RNS are predominantly implicated in causing cell damage, they also play a major physiological role in several aspects of intracellular signalling and regulation. ROS/RNS are known to play a dual role in biological systems since they can be either harmful or beneficial to living systems.

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Nitric oxide donors release extracellular traps from human neutrophils by augmenting free radical generation

Cited by 138 publications

References 51 publications

HMGB1 promotes neutrophil extracellular trap formation through interactions with Toll-like receptor 4

HMGB1 promotes neutrophil extracellular trap formation through interactions with Toll-like receptor 4

NETosis: how vital is it?

Ageing:Consequences of Excessive Free Radicals and Inflammation

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