Evidence map›Paper›PMID 39253969›Full record

ArticleJCI insight2024

Emergence of dysfunctional neutrophils with a defect in arginase-1 release in severe COVID-19.

Amrita Dwivedi, Aisling Ui Mhaonaigh, Makala Carroll, Bahareh Khosravi, Isabella Batten, Robert Seán Ballantine, Stuart Hendricken Phelan, Laura O'Doherty, Angel Mary George, Jacklyn Sui and 9 more

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Cytosolic proliferating cell nuclear antigen (PCNA) orchestrates neutrophil hyperactivation in COVID-19.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Amrita DwivediTrinity Kidney Centre, School of Medicine, and.
Aisling Ui MhaonaighTrinity Kidney Centre, School of Medicine, and.
Makala CarrollTrinity Kidney Centre, School of Medicine, and.
Bahareh KhosraviTrinity Kidney Centre, School of Medicine, and.
Isabella BattenDepartment of Medical Gerontology, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland.
Robert Seán BallantineTrinity Kidney Centre, School of Medicine, and.
Stuart Hendricken PhelanWellcome Trust, Clinical Research Facility.
Laura O'DohertyWellcome Trust, Clinical Research Facility.
Angel Mary GeorgeDepartment of Immunology, St James's Hospital, Dublin, Ireland.
Jacklyn SuiDepartment of Medical Gerontology, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland.
Heike C HawerkampSchool of Medicine, Trinity Biomedical Sciences Institute.
Padraic G FallonSchool of Medicine, Trinity Biomedical Sciences Institute.
Elnè NoppeDepartment of Critical Care, Tallaght University Hospital, Trinity College Dublin, Dublin, Ireland.
Sabina MasonDepartment of Critical Care, Tallaght University Hospital, Trinity College Dublin, Dublin, Ireland.
Niall ConlonDepartment of Infectious Diseases; and.
Clíona Ni CheallaighDepartment of Infectious Diseases; and.
Conor M FinlayTrinity Kidney Centre, School of Medicine, and.
Mark A LittleTrinity Kidney Centre, School of Medicine, and.
On Behalf Of The St James's And Tallaght Trinity Allied Researchers Sttar BioresourceThe STTAR Bioresource is detailed in Supplemental Acknowledgments.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophilia occurs in patients infected with SARS-CoV-2 (COVID-19) and is predictive of poor outcomes. Here, we link heterogenous neutrophil populations to disease severity in COVID-19. We identified neutrophils with features of cellular aging and immunosuppressive capacity in mild COVID-19 and features of neutrophil immaturity and activation in severe disease. The low-density neutrophil (LDN) number in circulating blood correlated with COVID-19 severity. Many of the divergent neutrophil phenotypes in COVID-19 were overrepresented in the LDN fraction and were less detectable in normal-density neutrophils. Functionally, neutrophils from patients with severe COVID-19 displayed defects in neutrophil extracellular trap formation and reactive oxygen species production. Soluble factors secreted by neutrophils from these patients inhibited T cell proliferation. Neutrophils from patients with severe COVID-19 had increased expression of arginase-1 protein, a feature that was retained in convalescent patients. Despite this increase in intracellular expression, there was a reduction in arginase-1 release by neutrophils into serum and culture supernatants. Furthermore, neutrophil-mediated T cell suppression was independent of arginase-1. Our results indicate the presence of dysfunctional, activated, and immature neutrophils in severe COVID-19.

Indexed as

ArginaseCOVID-19NeutrophilsSARS-CoV-2Severity of Illness IndexAdultAgedExtracellular TrapsFemaleHumansMaleMiddle AgedNeutrophil ActivationReactive Oxygen SpeciesT-LymphocytesARG1 protein, humanArginaseReactive Oxygen SpeciesCOVID-19ImmunologyNeutrophils

Identifiers

PMID39253969
PMCPMC11385094

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.