ArticleIntensive care medicine experimental2014
Neutrophil extracellular traps in the host defense against sepsis induced by Burkholderia pseudomallei (melioidosis).
Article in Intensive care medicine experimental, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Immunology of Sepsis.Clinics in chest medicine · 2026Review
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- N-acetylcysteine inhibits NETs, exhibits antibacterial and antibiofilm properties and enhances neutrophil function against Burkholderia pseudomallei.Scientific reports · 2025Article
- Dysfunctional host cellular immune responses are associated with mortality in melioidosis.Emerging microbes & infections · 2024Article
- γδ T Cells Mediate Protection against Neutrophil-associated Lung Inflammation in Pulmonary Melioidosis.American journal of respiratory cell and molecular biology · 2024Article
- Circulating Nucleosomes as a Novel Biomarker for Sepsis: A Scoping Review.Biomedicines · 2024Article
- Burkholderia pseudomallei and melioidosis.Nature reviews. Microbiology · 2024Review
- Role of Extracellular Trap Release During Bacterial and Viral Infection.Frontiers in microbiology · 2022Review
- Zingerone Inhibits the Neutrophil Extracellular Trap Formation and Protects against Sepsis via Nrf2-Mediated ROS Inhibition.Oxidative medicine and cellular longevity · 2022Article
- Outer membrane vesicles from bacteria: Role and potential value in the pathogenesis of chronic respiratory diseases.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Hijacking of the Host's Immune Surveillance Radars byFrontiers in immunology · 2021Review
- Peptidylarginine Deiminase 2 in Host Immunity: Current Insights and Perspectives.Frontiers in immunology · 2021Review
- Peptidylarginine deiminase 2 has potential as both a biomarker and therapeutic target of sepsis.JCI insight · 2020Article
- Neutrophil Elastase and Neutrophil Extracellular Traps in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- Thrombocytopenia Impairs Host Defense Against Burkholderia pseudomallei (Melioidosis).The Journal of infectious diseases · 2019Article
- Neutrophil extracellular traps in immunity and disease.Nature reviews. Immunology · 2018Review
- Boosting of post-exposure human T-cell and B-cell recall responses in vivo by Burkholderia pseudomallei-related proteins.Immunology · 2017Article
- Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis.PLoS neglected tropical diseases · 2017Article
- Consequences of extracellular trap formation in sepsis.Current opinion in hematology · 2017Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeutrophil extracellular traps (NETs) are a central player in the host response to bacteria: neutrophils release extracellular DNA (nucleosomes) and neutrophil elastase to entrap and kill bacteria. We studied the role of NETs in Burkholderia pseudomallei infection (melioidosis), an important cause of Gram-negative sepsis in Southeast Asia.
methodsIn a prospective observational study, circulating nucleosomes and neutrophil elastase were assayed in 44 patients with Gram-negative sepsis caused by B. pseudomallei (melioidosis) and 82 controls. Functional assays included human neutrophil stimulation and killing assays and a murine model of B. pseudomallei infection in which NET function was compromised using DNase. Specified pathogen-free 8- to 12-week-old C57BL/6 mice were sacrificed post-infection to assess bacterial loads, inflammation, and pathology.
resultsNucleosome and neutrophil elastase levels were markedly elevated in patients compared to controls. NETs killed B. pseudomallei effectively, and neutrophils stimulated with B. pseudomallei showed increased elastase and DNA release in a time- and dose-dependent matter. In mice, NET disruption with intravenous DNase administration resulted in decreased nucleosome levels. Although DNase treatment of mice resulted in diminished liver inflammation, no differences were observed in bacterial dissemination or systemic inflammation.
conclusionB. pseudomallei is a potent inducer of NETosis which was reflected by greatly increased levels of NET-related components in melioidosis patients. Although NETs exhibited antibacterial activity against B. pseudomallei, NET formation did not protect against bacterial dissemination and inflammation during B. pseudomallei-induced sepsis.
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Registered trials
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