ArticleInfection and immunity2012
Neutrophil extracellular traps exhibit antibacterial activity against burkholderia pseudomallei and are influenced by bacterial and host factors.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 87 citations in OpenAlex.
- Diabetes Mellitus as a Risk Factor for Severe Disease and Mortality Among Patients with Melioidosis: A Systematic Review and Meta-Analysis.Life (Basel, Switzerland) · 2026Review
- Analysis of HERV-K (HML2) Expression in Colorectal Cancer Samples.Epigenomes · 2026Article
- SodA promotes immune evasion ofMicrobiology spectrum · 2026Article
- Neutrophil Extracellular Traps in Wound Healing of Diabetes: Mechanisms, Inducers, and Therapeutic Implications.Mediators of inflammation · 2026Review
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- Risk of Type 1 Diabetes Mellitus in SARS-CoV-2 Patients.Current diabetes reviews · 2025Review
- Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation.Cell host & microbe · 2024Article
- Burkholderia pseudomallei and melioidosis.Nature reviews. Microbiology · 2024Review
- Encapsulated Streptococcus suis impairs optimal neutrophil functions which are not rescued by priming with colony-stimulating factors.PloS one · 2024Article
- Neutrophil extracellular traps in bacterial infections and evasion strategies.Frontiers in immunology · 2024Review
- Dysfunctions of Neutrophils in the Peripheral Blood of Children with Cystic Fibrosis.Biomedicines · 2023Article
- Eating the Enemy: Mycoplasma Strategies to Evade Neutrophil Extracellular Traps (NETs) Promoting Bacterial Nucleotides Uptake and Inflammatory Damage.International journal of molecular sciences · 2022Review
- The liver in sepsis: molecular mechanism of liver failure and their potential for clinical translation.Molecular medicine (Cambridge, Mass.) · 2022Review
- Article
- Role of Extracellular Trap Release During Bacterial and Viral Infection.Frontiers in microbiology · 2022Review
- Type 1 Diabetes Mellitus in the SARS-CoV-2 Pandemic: Oxidative Stress as a Major Pathophysiological Mechanism Linked to Adverse Clinical Outcomes.Antioxidants (Basel, Switzerland) · 2021Review
- Hijacking of the Host's Immune Surveillance Radars byFrontiers in immunology · 2021Review
- Neutrophils: Need for Standardized Nomenclature.Frontiers in immunology · 2021Review
- Human Melioidosis.Clinical microbiology reviews · 2020Review
- Long non-coding RNA X-inactive specific transcript silencing ameliorates primary graft dysfunction following lung transplantation through microRNA-21-dependent mechanism.EBioMedicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 4 countries.
Funding
Abstract
Burkholderia pseudomallei is the causative pathogen of melioidosis, of which a major predisposing factor is diabetes mellitus. Polymorphonuclear neutrophils (PMNs) kill microbes extracellularly by the release of neutrophil extracellular traps (NETs). PMNs play a key role in the control of melioidosis, but the involvement of NETs in killing of B. pseudomallei remains obscure. Here, we showed that bactericidal NETs were released from human PMNs in response to B. pseudomallei in a dose- and time-dependent manner. B. pseudomallei-induced NET formation required NADPH oxidase activation but not phosphatidylinositol-3 kinase, mitogen-activated protein kinases, or Src family kinase signaling pathways. B. pseudomallei mutants defective in the virulence-associated Bsa type III protein secretion system (T3SS) or capsular polysaccharide I (CPS-I) induced elevated levels of NETs. NET induction by such mutants was associated with increased bacterial killing, phagocytosis, and oxidative burst by PMNs. Taken together the data imply that T3SS and the capsule may play a role in evading the induction of NETs. Importantly, PMNs from diabetic subjects released NETs at a lower level than PMNs from healthy subjects. Modulation of NET formation may therefore be associated with the pathogenesis and control of melioidosis.
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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.