Evidence map›Paper›PMID 25092706›Full record

ArticleAntimicrobial agents and chemotherapy2014

Inhibition of cyclooxygenase-1 and cyclooxygenase-2 impairs Trypanosoma cruzi entry into cardiac cells and promotes differential modulation of the inflammatory response.

Aparecida D Malvezi, Carolina Panis, Rosiane V da Silva, Rafael Carvalho de Freitas, Maria I Lovo-Martins, Vera L H Tatakihara, Nágela G Zanluqui, Edecio Cunha Neto, Samuel Goldenberg, Juliano Bordignon and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

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  11. Review
  12. Review
  13. Response toFrontiers in microbiology · 2017
    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

14 authors at 3 institutions in 1 country.

Aparecida D MalveziLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Carolina PanisLaboratório de Patofisiologia e Radicais Livres, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Rosiane V da SilvaLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Rafael Carvalho de FreitasLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Maria I Lovo-MartinsLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Vera L H TatakiharaLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Nágela G ZanluquiLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Edecio Cunha NetoLaboratório de Immunologia, Instituto do Coração, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Samuel GoldenbergInstituto Carlos Chagas/Fiocruz, Curitiba, Brazil.
Juliano BordignonInstituto Carlos Chagas/Fiocruz, Curitiba, Brazil.
Sueli F Yamada-OgattaLaboratório de Biologia Molecular de Microrganismos, Departamento de Microbiologia, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Marli C Martins-PingeDepartamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Rubens CecchiniLaboratório de Patofisiologia e Radicais Livres, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Phileno Pinge-FilhoLaboratório de Imunopatologia Experimental, Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil pingefilho@uel.br.
Universidade Estadual de Londrina · BRFundação Carlos Chagas · BRHospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intracellular protozoan parasite Trypanosoma cruzi is the etiologic agent of Chagas disease, a serious disorder that affects millions of people in Latin America. Cell invasion by T. cruzi and its intracellular replication are essential to the parasite's life cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host's cyclooxygenase (COX) enzymes during T. cruzi invasion. Pharmacological antagonists for COX-1 (aspirin) and COX-2 (celecoxib) caused marked inhibition of T. cruzi infection when rat cardiac cells were pretreated with these nonsteroidal anti-inflammatory drugs (NSAIDs) for 60 min at 37°C before inoculation. This inhibition was associated with an increase in the production of NO and interleukin-1β and decreased production of transforming growth factor β (TGF-β) by cells. Taken together, these results indicate that COX-1 more than COX-2 is involved in the regulation of anti-T. cruzi activity in cardiac cells, and they provide a better understanding of the influence of TGF-β-interfering therapies on the innate inflammatory response to T. cruzi infection and may represent a very pertinent target for new therapeutic treatments of Chagas disease.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalAspirinCelecoxibCell LineCells, CulturedCell SurvivalCyclooxygenase 1Cyclooxygenase 2Enzyme-Linked Immunosorbent AssayImmunity, InnateImmunohistochemistryInterleukin-1betaMyoblasts, CardiacNitric OxidePyrazolesAnti-Inflammatory Agents, Non-SteroidalAspirinCelecoxibCyclooxygenase 1Cyclooxygenase 2Interleukin-1betaNitric OxidePyrazolesSulfonamidesTransforming Growth Factor alphaTransforming Growth Factor beta

Identifiers

PMID25092706
PMCPMC4187892
OpenAlexW2157672004

What OpenQuestion holds

Textmetadata
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.