Evidence map›Paper›PMID 36864506›Full record

ArticleRespiratory research2023

Targeting neutrophils extracellular traps (NETs) reduces multiple organ injury in a COVID-19 mouse model.

Flavio P Veras, Giovanni F Gomes, Bruna M S Silva, Diego B Caetité, Cicero J L R Almeida, Camila Meirelles S Silva, Ayda H Schneider, Emily S Corneo, Caio S Bonilha, Sabrina S Batah and 6 more

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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  13. Lipid nanoparticles target neutrophils to reduce SARS-CoV-2-induced lung injury and inflammation.Journal of controlled release : official journal of the Controlled Release Society · 2025
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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

16 authors at 3 institutions in 1 country.

Flavio P VerasCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil. fprotasio@usp.br.
Giovanni F GomesCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Bruna M S SilvaCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Diego B CaetitéCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Cicero J L R AlmeidaCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Camila Meirelles S SilvaCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Ayda H SchneiderCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Emily S CorneoLaboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, Santa Catarina, Brazil.
Caio S BonilhaCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Sabrina S BatahDepartment of Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Ronaldo MartinsVirology Research Center, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Eurico ArrudaVirology Research Center, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Alexandre T FabroDepartment of Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
José C Alves-FilhoCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Thiago M CunhaCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Fernando Q CunhaCenter of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes; Rua das Paineiras, Casa 3, Ribeirão Preto, São Paulo, 14049-900, Brazil. fdqcunha@fmrp.usp.br.
Universidade de São Paulo · BRClinics Hospital of Ribeirão Preto · BRUniversidade do Sul de Santa Catarina · BR

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 88887.513530/2020-00Fundação de Amparo à Pesquisa do Estado de São Paulo 2013/08216-2
6 · The paper itself

Abstract

backgroundCOVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment.

methodsHere, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers.

resultsDNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I.

conclusionsTogether, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes.

Indexed as

Acute Lung InjuryCOVID-19Extracellular TrapsAnimalsCOVID-19 Drug TreatmentDeoxyribonuclease IDisease Models, Animalgamma-GlobulinsHumansMelphalanMiceNeutrophilsSARS-CoV-2Deoxyribonuclease Igamma-GlobulinsK-18 conjugateMelphalanCOVID-19Neutrophil extracellular trapsNeutrophilsOrgan damageSARS-CoV-2

Identifiers

PMID36864506
PMCPMC9978286
OpenAlexW4322772207

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.