ArticleJournal of translational medicine2024
Impaired balance between neutrophil extracellular trap formation and degradation by DNases in COVID-19 disease.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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.
Biological Samples Collection From Patients and Caregivers Treated at Bordeaux University Hospital for Asymptomatic and Symptomatic Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) Infection (COVID-19).
Randomized Trial to Evaluate the Safety and Efficacy of Outpatient Treatments to Reduce the Risk of Worsening in Individuals With COVID-19 With Risk Factors (COVERAGE France)
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- From immunological mechanisms to targeted therapies: a bibliometric analysis in the domain of research concerning neutrophil extracellular traps and pulmonary diseases (2006-2025).Frontiers in immunology · 2026Pooled it
- sST2 is a key outcome biomarker in COVID-19: insights from discovery randomized trial.Scientific reports · 2025Trial
- NETs drive CD4⁺ T cell dysfunction in sepsis via mitochondrial ROS and impaired calcium signalling.Molecular medicine (Cambridge, Mass.) · 2026Article
- Silent Myocardial Infarction Revisited: Immuno-metabolic Mechanisms, Multimodal Biomarkers, and Translational Diagnostics.Journal of cardiovascular translational research · 2026Review
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Identification of Shared Gene Signatures Associated with Alzheimer's Disease and COVID-19 through Bioinformatics Analysis.Combinatorial chemistry & high throughput screening · 2026Article
- Neutrophil extracellular traps in gout: from immune defense to pathological dynamic equilibrium.Frontiers in immunology · 2026Review
- Cell-free DNA in sepsis: from molecular insights to clinical management.Military Medical Research · 2025Review
- Pulmonary and Immune Dysfunction in Pediatric Long COVID: A Case Study Evaluating the Utility of ChatGPT-4 for Analyzing Scientific Articles.Journal of clinical medicine · 2025Review
- Unraveling NETs in Sepsis: From Cellular Mechanisms to Clinical Relevance.International journal of molecular sciences · 2025Review
- Neutrophils secrete exosome-associated DNA to resolve sterile acute inflammation.Nature cell biology · 2025Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Biological mechanisms of pulmonary inflammation and its association with seropositive rheumatoid arthritis.Frontiers in immunology · 2025Review
- Neutrophil extracellular traps and macrophage activation contibute to thrombosis and post-covid syndrome in SARS-CoV-2 infection.Frontiers in immunology · 2025Article
- Dual-functional cerium oxide nanoparticles with antioxidant and DNase I activities to prevent and degrade neutrophil extracellular traps.Frontiers in immunology · 2025Article
- Different results despite high homology: Comparative expression of human and murine DNase1 in Pichia pastoris.PloS one · 2025Article
- Post-COVID pulmonary injury in K18-hACE2 mice shows persistent neutrophils and neutrophil extracellular trap formation.Immunity, inflammation and disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThrombo-inflammation and neutrophil extracellular traps (NETs) are exacerbated in severe cases of COVID-19, potentially contributing to disease exacerbation. However, the mechanisms underpinning this dysregulation remain elusive. We hypothesised that lower DNase activity may be associated with higher NETosis and clinical worsening in patients with COVID-19.
methodsBiological samples were obtained from hospitalized patients (15 severe, 37 critical at sampling) and 93 non-severe ambulatory cases. Our aims were to compare NET biomarkers, functional DNase levels, and explore mechanisms driving any imbalance concerning disease severity.
resultsFunctional DNase levels were diminished in the most severe patients, paralleling an imbalance between NET markers and DNase activity. DNase1 antigen levels were higher in ambulatory cases but lower in severe patients. DNase1L3 antigen levels remained consistent across subgroups, not rising alongside NET markers. DNASE1 polymorphisms correlated with reduced DNase1 antigen levels. Moreover, a quantitative deficiency in plasmacytoid dendritic cells (pDCs), which primarily express DNase1L3, was observed in critical patients. Analysis of public single-cell RNAseq data revealed reduced DNase1L3 expression in pDCs from severe COVID-19 patient.
conclusionSevere and critical COVID-19 cases exhibited an imbalance between NET and DNase functional activity and quantity. Early identification of NETosis imbalance could guide targeted therapies against thrombo-inflammation in COVID-19-related sepsis, such as DNase administration, to avert clinical deterioration.
trial registrationCOVERAGE trial (NCT04356495) and COLCOV19-BX study (NCT04332016).
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What OpenQuestion holds
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.