Evidence map›Paper›PMID 36239164›Full record

ReviewEuropean journal of immunology2023

Neutrophil activation and neutrophil extracellular traps (NETs) in COVID-19 ARDS and immunothrombosis.

Maria Candida Cesta, Mara Zippoli, Carolina Marsiglia, Elizabeth M Gavioli, Giada Cremonesi, Akram Khan, Flavio Mantelli, Marcello Allegretti, Robert Balk

Open access · hybridAbstract readReview
In one paragraph

Review in European journal of immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 2 pooled it
10.2field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 108 citations in OpenAlex.

  1. Pooled it
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  3. Diminished plasma levels of GPIb-Frontiers in medicine · 2026
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  9. Acta pharmaceutica Sinica. B · 2026
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7 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 2 countries.

Maria Candida CestaDompé farmaceutici SpA, L'Aquila, Italy.ORCID 0000-0002-4847-2985
Mara ZippoliDompé farmaceutici SpA, Napoli, Italy.ORCID 0000-0003-3749-1176
Carolina MarsigliaDompé farmaceutici SpA, L'Aquila, Italy.ORCID 0000-0002-4510-9582
Elizabeth M GavioliDompé U.S. Inc., Boston, USA.
Giada CremonesiDompé Farmaceutici S.p.A., Milano, Italy.
Akram KhanDivision of Pulmonary, and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon, USA.ORCID 0000-0003-3091-632X
Flavio MantelliDompé farmaceutici SpA, L'Aquila, Italy.
Marcello AllegrettiDompé farmaceutici SpA, L'Aquila, Italy.
Robert BalkDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Rush Medical College and Rush University Medical Center, Chicago, Illinois, USA.
Dompé (Italy) · ITBoston University · USOregon Health & Science University · USRush University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) is an acute inflammatory condition with a dramatic increase in incidence since the beginning of the coronavirus disease 19 (COVID-19) pandemic. Neutrophils play a vital role in the immunopathology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection by triggering the formation of neutrophil extracellular traps (NETs), producing cytokines including interleukin-8 (CXCL8), and mediating the recruitment of other immune cells to regulate processes such as acute and chronic inflammation, which can lead to ARDS. CXCL8 is involved in the recruitment, activation, and degranulation of neutrophils, and therefore contributes to inflammation amplification and severity of disease. Furthermore, activation of neutrophils also supports a prothrombotic phenotype, which may explain the development of immunothrombosis observed in COVID-19 ARDS. This review aims to describe hyperinflammatory ARDS due to SARS-CoV-2 infection. In addition, we address the critical role of polymorphonuclear neutrophils, inflammatory cytokines, and the potential targeting of CXCL8 in treating the hyperinflammatory ARDS population.

Indexed as

COVID-19Extracellular TrapsRespiratory Distress SyndromeCytokinesHumansInflammationNeutrophil ActivationNeutrophilsSARS-CoV-2ThromboinflammationCytokinesARDSCOVID-19CXCL8immunomodulators

Identifiers

PMID36239164
PMCPMC9874644
OpenAlexW4306165498

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.