Evidence map›Paper›PMID 31706334›Full record

ArticleParasites & vectors2019

Effects of ghrelin supplementation on the acute phase of Chagas disease in rats.

Ferdinando de Paula Silva, Cássia Mariana Bronzon da Costa, Luiz Miguel Pereira, Diego Fernando Silva Lessa, Dimitrius Leonardo Pitol, João Paulo Mardegan Issa, José Clóvis do Prado Júnior, Ana Amélia Carraro Abrahão

Open access · goldAbstract read
In one paragraph

Article in Parasites & vectors, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

8 authors at 2 institutions in 1 country.

Ferdinando de Paula SilvaDepartment of Clinical Analyses, Toxicology and Food Science, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14040-903, Brazil.
Cássia Mariana Bronzon da CostaDepartment of Clinical Analyses, Toxicology and Food Science, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14040-903, Brazil.ORCID http://orcid.org/0000-0002-2860-4290
Luiz Miguel PereiraDepartment of Clinical Analyses, Toxicology and Food Science, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14040-903, Brazil.
Diego Fernando Silva LessaDepartment of Clinical Analyses, Toxicology and Food Science, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14040-903, Brazil.
Dimitrius Leonardo PitolDepartment of Morphology, Physiology and Basic Pathology, School of Dentistry of Ribeirão Preto USP, University of São Paulo, Ribeirão Preto, 14040-904, Brazil.
João Paulo Mardegan IssaDepartment of Morphology, Physiology and Basic Pathology, School of Dentistry of Ribeirão Preto USP, University of São Paulo, Ribeirão Preto, 14040-904, Brazil.
José Clóvis do Prado JúniorDepartment of Clinical Analyses, Toxicology and Food Science, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14040-903, Brazil.
Ana Amélia Carraro AbrahãoDepartment of Clinical Analyses, Toxicology and Food Science, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, 14040-903, Brazil. acarraro@fcfrp.usp.br.
Universidade de São Paulo · BRUniversidade de Ribeirão Preto · BR

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Finance Code 001Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/18682-3
6 · The paper itself

Abstract

backgroundTrypanosoma cruzi is the causative agent of Chagas disease, which is endemic to subtropical and tropical Americas. The disease treatment remains partially ineffective, involving therapies directed to the parasite as well as palliative strategies for the clinical manifestations. Therefore, novel candidates for disease control are necessary. Additionally, strategies based on parasite inhibition via specific targets and application of compounds which improve the immune response against the disease is welcomed. Ghrelin is a peptide hormone pointed as a substance with important cardioprotective, vasodilatory, anti-apoptotic, anti-oxidative and immune modulatory functions. The aims of this study were to evaluate the immunomodulatory effects of ghrelin in male Wistar rats infected with the Y strain of T. cruzi.

methodsIn order to delineate an immune response against T. cruzi mediated by ghrelin, we evaluated the following parameters: quantification of blood and cardiac parasites; analysis of cell markers (CD3

resultsThe animals infected with T. cruzi and supplemented with ghrelin demonstrated an upregulated pattern in macrophage and NO production, whereas an anti-inflammatory response was observed in T cells and cytokines. The low response against T. cruzi mediated by T cells probably contributed to a higher colonization of the cardiac tissue, when compared to infected groups. On the other side, the peptide decreased the inflammatory infiltration in cardiac tissue infected with T. cruzi.

conclusionsGhrelin demonstrated a dual function in animals infected with T. cruzi. Further studies, especially related to the decrease of cardiac tissue inflammation, are needed in order to determine the advantages of ghrelin supplementation in Chagas disease, mostly for populations from endemic areas.

Indexed as

AnimalsCardiotonic AgentsCell ProliferationChagas DiseaseCytokinesDisease Models, AnimalGhrelinImmunologic FactorsInjections, SubcutaneousLymphocytesMacrophagesMaleMyocardiumParasite LoadRats, WistarTreatment OutcomeCardiotonic AgentsCytokinesGhrelinImmunologic FactorsChagas diseaseGhrelinImmune responseInflammation

Identifiers

PMID31706334
PMCPMC6842500
OpenAlexW2988798514

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.