Evidence map›Paper›PMID 38097207›Full record

Observational studyThe European respiratory journal2024

Extensive acute and sustained changes to neutrophil proteomes post-SARS-CoV-2 infection.

Merete B Long, Andrew J M Howden, Holly R Keir, Christina M Rollings, Yan Hui Giam, Thomas Pembridge, Lilia Delgado, Hani Abo-Leyah, Amy F Lloyd, Gabriel Sollberger and 11 more

Open access · greenAbstract readObservational Study
In one paragraph

Observational study in The European respiratory journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
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, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 2 institutions in 3 countries.

Merete B LongDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Andrew J M HowdenDivision of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK.
Holly R KeirDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.ORCID https://orcid.org/0000-0001-7197-701X
Christina M RollingsDivision of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK.
Yan Hui GiamDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Thomas PembridgeDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Lilia DelgadoDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.ORCID https://orcid.org/0000-0002-0337-9189
Hani Abo-LeyahDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Amy F LloydDivision of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK.
Gabriel SollbergerDivision of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK.
Rebecca HullDepartment of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
Amy GilmourDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Chloe HughesDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Benjamin J M NewDepartment of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
Diane CassidyDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Amelia ShoemarkDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.ORCID https://orcid.org/0000-0001-7360-6060
Hollian RichardsonDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Angus I LamondDivision of Molecular, Cell and Developmental Biology, School of Life Sciences, University of Dundee, Dundee, UK.
Doreen A CantrellDivision of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK.
James D ChalmersDivision of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK j.chalmers@dundee.ac.uk.
Alejandro J BrenesDivision of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK.ORCID https://orcid.org/0000-0001-8298-2463
University of Dundee · GBUniversity of Sheffield · GB

Funding

Chief Scientist Office COV/DUN/20/01Chief Scientist Office COV/DUN/20/04Medical Research Council MC_PC_19034Wellcome Trust 205023/Z/16/Z
6 · The paper itself

Abstract

backgroundNeutrophils are important in the pathophysiology of coronavirus disease 2019 (COVID-19), but the molecular changes contributing to altered neutrophil phenotypes following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are not fully understood. We used quantitative mass spectrometry-based proteomics to explore neutrophil phenotypes immediately following acute SARS-CoV-2 infection and during recovery.

methodsProspective observational study of hospitalised patients with PCR-confirmed SARS-CoV-2 infection (May to December 2020). Patients were enrolled within 96 h of admission, with longitudinal sampling up to 29 days. Control groups comprised non-COVID-19 acute lower respiratory tract infection (LRTI) and age-matched noninfected controls. Neutrophils were isolated from peripheral blood and analysed using mass spectrometry. COVID-19 severity and recovery were defined using the World Health Organization ordinal scale.

resultsNeutrophil proteomes from 84 COVID-19 patients were compared to those from 91 LRTI and 42 control participants. 5800 neutrophil proteins were identified, with >1700 proteins significantly changed in neutrophils from COVID-19 patients compared to noninfected controls. Neutrophils from COVID-19 patients initially all demonstrated a strong interferon signature, but this signature rapidly declined in patients with severe disease. Severe disease was associated with increased abundance of proteins involved in metabolism, immunosuppression and pattern recognition, while delayed recovery from COVID-19 was associated with decreased granule components and reduced abundance of metabolic proteins, chemokine and leukotriene receptors, integrins and inhibitory receptors.

conclusionsSARS-CoV-2 infection results in the sustained presence of circulating neutrophils with distinct proteomes suggesting altered metabolic and immunosuppressive profiles and altered capacities to respond to migratory signals and cues from other immune cells, pathogens or cytokines.

Indexed as

COVID-19CytokinesHumansNeutrophilsProteomeSARS-CoV-2CytokinesProteome

Identifiers

PMID38097207
PMCPMC10918319
OpenAlexW4389727382

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.