Evidence map›Paper›PMID 40292988›Full record

ArticleEuropean journal of clinical investigation2025

Bosutinib mitigates inflammation in experimental sepsis.

C M C Cunha, V H P Abreu, V Estato, G M V Soares, B P T Moraes, G P Oliveira, J D Silva, P L Silva, R Immler, P R Rocco and 5 more

Abstract read
In one paragraph

Article in European journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Bosutinib mitigates inflammation in experimental sepsis.European journal of clinical investigation · 2025
    Article
  3. Article
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

15 authors.

C M C CunhaLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
V H P AbreuLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
V EstatoLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
G M V SoaresLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
B P T MoraesLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
G P OliveiraLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
J D SilvaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
P L SilvaLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
R ImmlerWalter Brendel Centre, Department of Cardiovascular Physiology and Pathophysiology, Klinikum der Universität, Ludwig Maximilians University München, Munich, Germany.
P R RoccoLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
M SperandioWalter Brendel Centre, Department of Cardiovascular Physiology and Pathophysiology, Klinikum der Universität, Ludwig Maximilians University München, Munich, Germany.ORCID https://orcid.org/0000-0002-7689-3613
A R SilvaLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
P T BozzaLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.ORCID https://orcid.org/0000-0001-8349-9529
H C Castro-Faria-NetoLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
C F Gonçalves-de-AlbuquerqueLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.ORCID https://orcid.org/0000-0002-4458-3055

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) 001Deutsche Forschungsgemeinschaft (DFG) TRR332 #449437943Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) E-26/010.000983/2019Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) E-26/2010.592/2019Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) E-26/201.448/2021Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) E-26/203.290/2017Instituto Oswaldo Cruz, FIOCRUZPrograma de Biotecnologia da Universidade Federal Fluminense (UFF)Programa de Pós Graduação em Biologia Molecular Celular (UNIRIO)Universidade Federal do Estado do Rio de Janeiro (UNIRIO)Universidade Federal Fluminense (PROPPI/UFF)
6 · The paper itself

Abstract

backgroundSepsis, a leading cause of death globally, lacks targeted and effective treatment. Its pathophysiology involves unbalanced inflammation, marked by a high release of inflammatory mediators, leukocyte recruitment, vascular changes and dysfunction of the nervous and respiratory systems. Src family tyrosine kinases (SFK) play a critical role in immune responses, and their inhibition can modulate excessive inflammation. This study investigates the potential of bosutinib, an SFK inhibitor, as a treatment for sepsis.

methodsClinical signs, survival rates, systemic and neuronal inflammatory responses, cell recruitment, lung function and cerebral microcirculation were analysed in mice treated with bosutinib (3 mg/kg) or DMSO/saline followed by cecal ligation and puncture (CLP)-induced sepsis.

resultsBosutinib treatment reduced the severity of sepsis, improved survival rates and reduced the levels of pro-inflammatory cytokines and chemokines in peritoneal lavage, plasma and brain tissue. It also reduced cellular infiltration and bacterial growth at the infection site and protected lung function by reducing diffuse alveolar damage. Using intravital microscopy and laser speckle techniques, bosutinib improved capillary density and blood perfusion and reduced leukocyte recruitment and adhesion in the cerebral microcirculation of septic animals.

conclusionsBosutinib pretreatment attenuated dysregulated inflammatory responses and neurovascular changes in experimental sepsis.

Indexed as

Aniline CompoundsInflammationNitrilesProtein Kinase InhibitorsQuinolinesSepsissrc-Family KinasesAnimalsCerebrovascular CirculationChemokinesCytokinesDisease Models, AnimalMaleMiceMice, Inbred C57BLMicrocirculationAniline CompoundsbosutinibChemokinesCytokinesNitrilesProtein Kinase InhibitorsQuinolinessrc-Family KinasesbosutinibneuroinflammationsepsisSrc family tyrosine kinase inhibitors

Identifiers

PMID40292988
PMCPMC12362053

What OpenQuestion holds

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LicenceCC BY
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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.