ArticlePloS one2013
Pyocyanin-enhanced neutrophil extracellular trap formation requires the NADPH oxidase.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 128 citations in OpenAlex.
- Release of cystic fibrosis airway inflammatory markers from Pseudomonas aeruginosa-stimulated human neutrophils involves NADPH oxidase-dependent extracellular DNA trap formation.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Targeting neutrophil extracellular traps in bacterial infections: mechanistic insights and translational perspectives.Frontiers in immunology · 2026Review
- N-acetylcysteine inhibits NETs, exhibits antibacterial and antibiofilm properties and enhances neutrophil function against Burkholderia pseudomallei.Scientific reports · 2025Article
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- Anaeic and tumoic acids, new functionalized fatty acids from marine cyanobacteria, inhibit quorum sensing inMedicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2025Article
- The adaptability ofFrontiers in cellular and infection microbiology · 2025Review
- Review
- Modulation of pulmonary immune functions by theFrontiers in immunology · 2025Review
- Equine neutrophils selectively release neutrophil extracellular traps in response to chemical and bacterial agonists.Frontiers in veterinary science · 2025Article
- Flagellum-deficientMicrobiology spectrum · 2024Article
- Neutrophil extracellular traps in bacterial infections and evasion strategies.Frontiers in immunology · 2024Review
- Alterations of oral microbiome and metabolic signatures and their interaction in oral lichen planus.Journal of oral microbiology · 2024Article
- Host-microbe interactions in chronic rhinosinusitis biofilms and models for investigation.Biofilm · 2023Review
- Common mechanisms underlying diabetic vascular complications: focus on the interaction of metabolic disorders, immuno-inflammation, and endothelial dysfunction.Cell communication and signaling : CCS · 2023Review
- Dysfunctions of Neutrophils in the Peripheral Blood of Children with Cystic Fibrosis.Biomedicines · 2023Article
- Attenuation of LPS-Induced Lung Injury by Benziodarone via Reactive Oxygen Species Reduction.International journal of molecular sciences · 2023Article
- Neutrophil extracellular traps and long COVID.Frontiers in immunology · 2023Review
- Caspase-1-driven neutrophil pyroptosis and its role in host susceptibility to Pseudomonas aeruginosa.PLoS pathogens · 2022Article
- Human Intelectin-1 Promotes Cellular Attachment and Neutrophil Killing of Streptococcus pneumoniae in a Serotype-Dependent Manner.Infection and immunity · 2022Article
- Environmental, Microbiological, and Immunological Features of Bacterial Biofilms Associated with Implanted Medical Devices.Clinical microbiology reviews · 2022Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Beyond intracellular killing, a novel neutrophil-based antimicrobial mechanism has been recently discovered: entrapment and killing by neutrophil extracellular traps (NETs). NETs consist of extruded nuclear DNA webs decorated with granule proteins. Although NET formation is an important innate immune mechanism, uncontrolled NET release damages host tissues and has been linked to several diseases including cystic fibrosis (CF). The major CF airway pathogen Pseudomonas aeruginosa establishes chronic infection. Pseudomonas imbedded within biofilms is protected against the immune system, but maintains chronic inflammation that worsens disease symptoms. Aberrant NET release from recruited neutrophils was found in CF, but the underlying mechanisms remain unclear. One of the most important Pseudomonas virulence factors is pyocyanin, a redox-active pigment that has been associated with diminished lung function in CF. Here we show that pyocyanin promotes NET formation in a time- and dose-dependent manner. Most CF Pseudomonas clinical isolates tested produce pyocyanin in vitro. Pyocyanin-derived reactive oxygen species are required for its NET release. Inhibitor experiments demonstrated involvement of Jun N-terminal Kinase (JNK) and phosphatidylinositol 3-Kinase (PI3K) in pyocyanin-induced NET formation. Pyocyanin-induced NETs also require the NADPH oxidase because NET release in chronic granulomatous disease neutrophils was greatly reduced. Comparison of neutrophils from gp91phox- and p47phox-deficient patients revealed that pyocyanin-triggered NET formation is proportional to their residual superoxide production. Our studies identify pyocyanin as the first secreted bacterial toxin that enhances NET formation. The involvement of NADPH oxidase in pyocyanin-induced NET formation represents a novel mechanism of pyocyanin toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.