Trial reportJCI insight2022
A functionally distinct neutrophil landscape in severe COVID-19 reveals opportunities for adjunctive therapies.
Trial report in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 41 citations in OpenAlex.
- Clinical Phenotyping in Acute Respiratory Distress Syndrome: Steps Towards Personalized Medicine.Journal of clinical medicine · 2025Article
- Spatiotemporal regulation of neutrophil heterogeneity in health and disease.Human molecular genetics · 2025Review
- Epigenetic Regulation of Neutrophils in ARDS.Cells · 2025Review
- Emergence of dysfunctional neutrophils with a defect in arginase-1 release in severe COVID-19.JCI insight · 2024Article
- Extensive acute and sustained changes to neutrophil proteomes post-SARS-CoV-2 infection.The European respiratory journal · 2024Observational
- A GPCR-neuropeptide axis dampens hyperactive neutrophils by promoting an alternative-like polarization during bacterial infection.Immunity · 2024Article
- A Narrative Review: The Role of NETs in Acute Respiratory Distress Syndrome/Acute Lung Injury.International journal of molecular sciences · 2024Review
- MAFB shapes human monocyte-derived macrophage response to SARS-CoV-2 and controls severe COVID-19 biomarker expression.JCI insight · 2023Article
- How Neutrophils Shape the Immune Response: Reassessing Their Multifaceted Role in Health and Disease.International journal of molecular sciences · 2023Review
- Mitochondrial N-formyl methionine peptides contribute to exaggerated neutrophil activation in patients with COVID-19.Virulence · 2023Article
- Heat shock protein 27 in the pathogenesis of COVID-19 and non-COVID acute respiratory distress syndrome.Cell stress & chaperones · 2023Observational
- Article
- Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19.Journal of clinical immunology · 2023Article
- The comprehensive role of apoptosis inhibitor of macrophage (AIM) in pathological conditions.Clinical and experimental immunology · 2023Review
- Neutrophils during SARS-CoV-2 infection: Friend or foe?Immunological reviews · 2023Review
- Multi-omics of NET formation and correlations with CNDP1, PSPB, and L-cystine levels in severe and mild COVID-19 infections.Heliyon · 2023Article
- Neutrophil extracellular traps and long COVID.Frontiers in immunology · 2023Review
- COVID-19 immunopathology: From acute diseases to chronic sequelae.Journal of medical virology · 2023Review
- Neutrophil activation and neutrophil extracellular traps (NETs) in COVID-19 ARDS and immunothrombosis.European journal of immunology · 2023Review
- Single-Cell RNA Sequencing and Transcriptome Analysis Revealed the Immune Microenvironment and Gene Markers of Acute Respiratory Distress Syndrome.Journal of inflammation research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Acute respiratory distress syndrome (ARDS) is a life-threatening syndrome, constituted by respiratory failure and diffuse alveolar damage that results from dysregulated local and systemic immune activation, causing pulmonary vascular, parenchymal, and alveolar damage. SARS-CoV-2 infection has become the dominant cause of ARDS worldwide, and emerging evidence implicates neutrophils and their cytotoxic arsenal of effector functions as central drivers of immune-mediated lung injury in COVID-19 ARDS. However, key outstanding questions are whether COVID-19 drives a unique program of neutrophil activation or effector functions that contribute to the severe pathogenesis of this pandemic illness and whether this unique neutrophil response can be targeted to attenuate disease. Using a combination of high-dimensional single-cell analysis and ex vivo functional assays of neutrophils from patients with COVID-19 ARDS, compared with those with non-COVID ARDS (caused by bacterial pneumonia), we identified a functionally distinct landscape of neutrophil activation in COVID-19 ARDS that was intrinsically programmed during SARS-CoV-2 infection. Furthermore, neutrophils in COVID-19 ARDS were functionally primed to produce high amounts of neutrophil extracellular traps. Surprisingly, this unique pathological program of neutrophil priming escaped conventional therapy with dexamethasone, thereby revealing a promising target for adjunctive immunotherapy in severe COVID-19.
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.