Evidence map›Paper›PMID 31443678›Full record

ArticleStem cell research & therapy2019

Eicosapentaenoic acid potentiates the therapeutic effects of adipose tissue-derived mesenchymal stromal cells on lung and distal organ injury in experimental sepsis.

Johnatas D Silva, Miquéias Lopes-Pacheco, Ligia L de Castro, Jamil Z Kitoko, Stefano A Trivelin, Natália R Amorim, Vera L Capelozzi, Marcelo M Morales, Bianca Gutfilen, Sergio A L de Souza and 3 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.7field-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

29 citing papers in PubMed, 60 citations in OpenAlex.

  1. Bosutinib mitigates inflammation in experimental sepsis.European journal of clinical investigation · 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

13 authors at 4 institutions in 3 countries.

Johnatas D SilvaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Miquéias Lopes-PachecoLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Ligia L de CastroLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Jamil Z KitokoLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Stefano A TrivelinLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Natália R AmorimLaboratory of Inflammation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Vera L CapelozziDepartment of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil.
Marcelo M MoralesLaboratory of Cellular and Molecular Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Bianca GutfilenDepartment of Radiology, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Sergio A L de SouzaDepartment of Radiology, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Daniel J WeissDepartment of Medicine, College of Medicine, University of Vermont, Burlington, VT, USA.
Bruno L DiazLaboratory of Inflammation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Patricia R M RoccoLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil. prmrocco@gmail.com.ORCID 0000-0003-1412-7136
Universidade Federal do Rio de Janeiro · BRCzech Academy of Sciences, Institute of Biophysics · CZUniversidade de São Paulo · BRUniversity of Vermont · US

Funding

Mechanisms of CD8+ T Cell Dynamics in Recurrent Ocular Herpetic DiseaseR01EY026103 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI BENMOHAMED, LBACHIR · 2016 to 2019
$1.5M
6 · The paper itself

Abstract

backgroundEven though mesenchymal stromal cells (MSCs) mitigate lung and distal organ damage in experimental polymicrobial sepsis, mortality remains high. We investigated whether preconditioning with eicosapentaenoic acid (EPA) would potentiate MSC actions in experimental sepsis by further decreasing lung and distal organ injury, thereby improving survival.

methodsIn C57BL/6 mice, sepsis was induced by cecal hligation and puncture (CLP); sham-operated animals were used as control. Twenty-four hours after surgery, CLP mice were further randomized to receive saline, adipose tissue-derived (AD)-MSCs (10

resultsNonpreconditioned and EPA-preconditioned AD-MSCs exhibited similar viability and differentiation capacity, accumulated mainly in the lungs and kidneys following systemic administration. Compared to nonpreconditioned AD-MSCs, EPA-preconditioned AD-MSCs further reduced static lung elastance, alveolar collapse, interstitial edema, alveolar septal inflammation, collagen fiber content, neutrophil cell count as well as protein levels of interleukin-1β and keratinocyte chemoattractant in lung tissue, and morphological abnormalities in the heart (cardiac myocyte architecture), liver (hepatocyte disarrangement and Kupffer cell hyperplasia), kidney (acute tubular necrosis), spleen (increased number of megakaryocytes and lymphocytes), and small bowel (villi architecture disorganization). EPA preconditioning of MSCs resulted in increased secretion of pro-resolution and anti-inflammatory mediators (RvD

conclusionsCompared to nonpreconditioned cells, EPA-preconditioned AD-MSCs yielded further reductions in the lung and distal organ injury, resulting in greater improvement in sepsis severity score and higher survival rate in CLP-induced experimental sepsis. This may be a promising therapeutic approach to improve outcome in septic patients.

Indexed as

Adipose TissueAnimalsCombined Modality TherapyCytokinesEicosapentaenoic AcidInflammation MediatorsLung InjuryMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMice, Inbred C57BLSepsisCytokinesEicosapentaenoic AcidInflammation MediatorsEicosapentaenoic acidInflammationMacrophagesMesenchymal stromal cellsPreconditioningSepsis

Identifiers

PMID31443678
PMCPMC6708232
OpenAlexW2969828289

What OpenQuestion holds

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LicenceCC BY
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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.