ArticleCells2022
Severe COVID-19 Shares a Common Neutrophil Activation Signature with Other Acute Inflammatory States.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Immune transcriptomic differences in paediatric patients with SARS-CoV-2 compared to other lower respiratory tract infections.bioRxiv : the preprint server for biology · 2025Article
- Artificial intelligence and systems biology analysis in stem cell research and therapeutics development.Stem cells translational medicine · 2025Review
- Dysregulated autoantibodies targeting AGTR1 are associated with the accumulation of COVID-19 symptoms.NPJ systems biology and applications · 2025Article
- Cytokine-induced transcriptional changes in human neutrophils reveal immune regulatory plasticity.Discovery immunology · 2025Article
- Neutrophil gene expression in COVID-19 patients with acute respiratory distress syndrome.Frontiers in immunology · 2025Article
- Gene Expression Dysregulation in Whole Blood of Patients withInternational journal of molecular sciences · 2024Article
- Article
- Integrated analysis of RNA-seq datasets reveals novel targets and regulators of COVID-19 severity.Life science alliance · 2024Article
- Remodeling of the chromatin landscape in peripheral blood cells in patients with severe Delta COVID-19.Frontiers in immunology · 2024Article
- Exploring common pathogenic association between Epstein Barr virus infection and long-COVID by integrating RNA-Seq and molecular dynamics simulations.Frontiers in immunology · 2024Article
- Immunological signatures unveiled by integrative systems vaccinology characterization of dengue vaccination trials and natural infection.Frontiers in immunology · 2024Article
- Multisystem inflammatory syndrome in children (MIS-C): Implications for long COVID.Inflammopharmacology · 2023Review
- Innate immune dysregulation in multisystem inflammatory syndrome in children (MIS-C).Scientific reports · 2023Article
- Article
- Bioinformatics and system biology approach to identify potential common pathogenesis for COVID-19 infection and osteoarthritis.Scientific reports · 2023Article
- Multi-omic Profiling Reveals Early Immunological Indicators for Identifying COVID-19 Progressors.bioRxiv : the preprint server for biology · 2023Article
- Immunometabolic Signature during Respiratory Viral Infection: A Potential Target for Host-Directed Therapies.Viruses · 2023Review
- Integrative systems immunology uncovers molecular networks of the cell cycle that stratify COVID-19 severity.Journal of medical virology · 2023Article
- Identification of 3 key genes as novel diagnostic and therapeutic targets for OA and COVID-19.Frontiers in immunology · 2023Article
- Relationship between red blood cell aggregation and dextran molecular mass.Scientific reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors at 7 institutions in 5 countries.
Funding
Abstract
Severe COVID-19 patients present a clinical and laboratory overlap with other hyperinflammatory conditions such as hemophagocytic lymphohistiocytosis (HLH). However, the underlying mechanisms of these conditions remain to be explored. Here, we investigated the transcriptome of 1596 individuals, including patients with COVID-19 in comparison to healthy controls, other acute inflammatory states (HLH, multisystem inflammatory syndrome in children [MIS-C], Kawasaki disease [KD]), and different respiratory infections (seasonal coronavirus, influenza, bacterial pneumonia). We observed that COVID-19 and HLH share immunological pathways (cytokine/chemokine signaling and neutrophil-mediated immune responses), including gene signatures that stratify COVID-19 patients admitted to the intensive care unit (ICU) and COVID-19_nonICU patients. Of note, among the common differentially expressed genes (DEG), there is a cluster of neutrophil-associated genes that reflects a generalized hyperinflammatory state since it is also dysregulated in patients with KD and bacterial pneumonia. These genes are dysregulated at the protein level across several COVID-19 studies and form an interconnected network with differentially expressed plasma proteins that point to neutrophil hyperactivation in COVID-19 patients admitted to the intensive care unit. scRNAseq analysis indicated that these genes are specifically upregulated across different leukocyte populations, including lymphocyte subsets and immature neutrophils. Artificial intelligence modeling confirmed the strong association of these genes with COVID-19 severity. Thus, our work indicates putative therapeutic pathways for intervention.
Indexed as
Identifiers
What Socratic 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 Socratic graph.