Evidence map›Paper›PMID 29760707›Full record

ArticleFrontiers in immunology2018

The Yin and Yang of Tyrosine Kinase Inhibition During Experimental Polymicrobial Sepsis.

Cassiano Felippe Gonçalves-de-Albuquerque, Ina Rohwedder, Adriana Ribeiro Silva, Alessandra Silveira Ferreira, Angela R M Kurz, Céline Cougoule, Sarah Klapproth, Tanja Eggersmann, Johnatas D Silva, Gisele Pena de Oliveira and 10 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Bosutinib mitigates inflammation in experimental sepsis.European journal of clinical investigation · 2025
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  4. Integrated Artificial Intelligence and Physics-Based Methods for theMedicinal chemistry (Shariqah (United Arab Emirates)) · 2025
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  5. Article
  6. Review
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  8. Article
  9. Review
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  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Mediterranean Diet: Lipids, Inflammation, and Malaria Infection.International journal of molecular sciences · 2020
    Review
  20. Neutrophils as emerging therapeutic targets.Nature reviews. Drug discovery · 2020
    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

20 authors at 8 institutions in 4 countries.

Cassiano Felippe Gonçalves-de-AlbuquerqueLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
Ina RohwedderWalter Brendel Centre, Department of Cardiovascular Physiology and Pathophysiology, Klinikum der Universität, Ludwig Maximilians University München, Munich, Germany.
Adriana Ribeiro SilvaLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
Alessandra Silveira FerreiraLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
Angela R M KurzLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
Céline CougouleInstitut de Pharmacologie et de Biologie Structurale, IPBS, Université de Toulouse, CNRS, UPS, Toulouse, France.
Sarah KlapprothWalter Brendel Centre, Department of Cardiovascular Physiology and Pathophysiology, Klinikum der Universität, Ludwig Maximilians University München, Munich, Germany.
Tanja EggersmannWalter Brendel Centre, Department of Cardiovascular Physiology and Pathophysiology, Klinikum der Universität, Ludwig Maximilians University München, Munich, Germany.
Johnatas D SilvaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Gisele Pena de OliveiraLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Vera Luiza CapelozziLaboratório de Genômica Pulmonar, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Gabriel Gutfilen SchlesingerLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
Edlaine Rijo CostaLaboratorio de Farmacologia, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Rita de Cassia Elias Estrela MarinsInstitut de Pharmacologie et de Biologie Structurale, IPBS, Université de Toulouse, CNRS, UPS, Toulouse, France.
Attila MócsaiMTA-SE "Lendület" Inflammation Physiology Research Group, Department of Physiology, Semmelweis University, Budapest, Hungary.
Isabelle Maridonneau-PariniInstitut de Pharmacologie et de Biologie Structurale, IPBS, Université de Toulouse, CNRS, UPS, Toulouse, France.
Barbara WalzogWalter Brendel Centre, Department of Cardiovascular Physiology and Pathophysiology, Klinikum der Universität, Ludwig Maximilians University München, Munich, Germany.
Patricia Rieken Macedo RoccoLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Markus SperandioWalter Brendel Centre, Department of Cardiovascular Physiology and Pathophysiology, Klinikum der Universität, Ludwig Maximilians University München, Munich, Germany.
Hugo Caire de Castro-Faria-NetoLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
Ludwig-Maximilians-Universität München · DEFundação Oswaldo Cruz · BRUniversidade Federal do Rio de Janeiro · BRInstitut de Pharmacologie et de Biologie Structurale · FRSemmelweis University · HUUniversidade de São Paulo · BRUniversité Fédérale de Toulouse Midi-Pyrénées · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are the first cells of our immune system to arrive at the site of inflammation. They release cytokines, e.g., chemokines, to attract further immune cells, but also actively start to phagocytose and kill pathogens. In the case of sepsis, this tightly regulated host defense mechanism can become uncontrolled and hyperactive resulting in severe organ damage. Currently, no effective therapy is available to fight sepsis; therefore, novel treatment targets that could prevent excessive inflammatory responses are warranted. Src Family tyrosine Kinases (SFK), a group of tyrosine kinases, have been shown to play a major role in regulating immune cell recruitment and host defense. Leukocytes with SFK depletion display severe spreading and migration defects along with reduced cytokine production. Thus, we investigated the effects of dasatinib, a tyrosine kinase inhibitor, with a strong inhibitory capacity on SFKs during sterile inflammation and polymicrobial sepsis in mice. We found that dasatinib-treated mice displayed diminished leukocyte adhesion and extravasation in tumor necrosis factor-α-stimulated cremaster muscle venules

Indexed as

AnimalsCell AdhesionDasatinibDisease Models, AnimalMaleMiceNeutrophil InfiltrationProtein Kinase InhibitorsSepsissrc-Family KinasesDasatinibProtein Kinase Inhibitorssrc-Family Kinasesdasatinibinflammationleukocyte traffickingsepsisSrc tyrosine kinase

Identifiers

PMID29760707
PMCPMC5936983
OpenAlexW2800640305

What OpenQuestion holds

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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.