ArticleJournal of innate immunity2016
Induction of Neutrophil Extracellular Traps in Shiga Toxin-Associated Hemolytic Uremic Syndrome.
Article in Journal of innate immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
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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
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.
- The emerging role of immunothrombosis in paediatric conditions.Pediatric research · 2019Pooled it
- In vitro induction of NETosis: Comprehensive live imaging comparison and systematic review.PloS one · 2017Pooled it
- Neutrophil extracellular traps and acute kidney injury: a narrative review.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in the animal model of adenine-induced chronic kidney disease.PloS one · 2026Article
- Neutrophil and neutrophil extracellular traps in acute kidney injury: from mechanisms to treatments.Frontiers in immunology · 2025Review
- ADAMTS13 or Caplacizumab Reduces the Accumulation of Neutrophil Extracellular Traps and Thrombus in Whole Blood of COVID-19 Patients under Flow.Thrombosis and haemostasis · 2024Article
- Is Endothelial Activation a Critical Event in Thrombotic Thrombocytopenic Purpura?Journal of clinical medicine · 2023Review
- Assessment of interleukin-10 promoter variant (-1082A/G) and cytokine production in patients with hemolytic uremic syndrome.Frontiers in pediatrics · 2023Article
- Dynamics of Plasma and Urinary Extracellular DNA in Acute Kidney Injury.International journal of molecular sciences · 2022Article
- Neutrophil Extracellular Traps Induced by Shiga Toxin and Lipopolysaccharide-Treated Platelets Exacerbate Endothelial Cell Damage.Frontiers in cellular and infection microbiology · 2022Article
- Impact of Neutrophil Extracellular Traps on Thrombosis Formation: New Findings and Future Perspective.Frontiers in cellular and infection microbiology · 2022Review
- Shiga Toxin 2a Induces NETosis via NOX-Dependent Pathway.Biomedicines · 2021Article
- Blood neutrophils from children with COVID-19 exhibit both inflammatory and anti-inflammatory markers.EBioMedicine · 2021Observational
- Differential Outcome between BALB/c and C57BL/6 Mice after Escherichia coli O157:H7 Infection Is Associated with a Dissimilar Tolerance Mechanism.Infection and immunity · 2021Article
- The interplay between neutrophils, complement, and microthrombi in COVID-19.Best practice & research. Clinical rheumatology · 2021Review
- Human Glomerular Endothelial Cells Treated With Shiga Toxin Type 2 Activate γδ T Lymphocytes.Frontiers in cellular and infection microbiology · 2021Article
- Verotoxin Receptor-Based Pathology and Therapies.Frontiers in cellular and infection microbiology · 2020Review
- Extracellular DNA traps in inflammation, injury and healing.Nature reviews. Nephrology · 2019Review
- Neutrophil Extracellular Traps in the Establishment and Progression of Renal Diseases.Medicina (Kaunas, Lithuania) · 2019Review
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemolytic uremic syndrome (HUS), a vascular disease characterized by hemolytic anemia, thrombocytopenia, and acute renal failure, is caused by enterohemorrhagic Shiga toxin (Stx)-producing bacteria, which mainly affect children. Besides Stx, the inflammatory response mediated by neutrophils (PMN) is essential to HUS evolution. PMN can release neutrophil extracellular traps (NET) composed of DNA, histones, and other proteins. Since NET are involved in infectious and inflammatory diseases, the aim of this work was to investigate the contribution of NET to HUS. Plasma from HUS patients contained increased levels of circulating free-DNA and nucleosomes in comparison to plasma from healthy children. Neutrophils from HUS patients exhibited a greater capacity to undergo spontaneous NETosis. NET activated human glomerular endothelial cells, stimulating secretion of the proinflammatory cytokines IL-6 and IL-8. Stx induced PMN activation as judged by its ability to trigger reactive oxygen species production, increase CD11b and CD66b expression, and induce NETosis in PMN from healthy donors. During HUS, NET can contribute to the inflammatory response and thrombosis in the microvasculature and thus to renal failure. Intervention strategies to inhibit inflammatory mechanisms mediated by PMN, such as NETosis, could have a potential therapeutic impact towards amelioration of the severity of HUS.
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