Evidence map›Paper›PMID 36590580›Full record

ArticleFrontiers in cellular and infection microbiology2022

An induced population of

Izadora Volpato Rossi, Maria Alice Ferreira Nunes, Bruna Sabatke, Hennrique Taborda Ribas, Sheila Maria Brochado Winnischofer, Augusto Savio Peixoto Ramos, Jameel Malhador Inal, Marcel Ivan Ramirez

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2022. 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
0.9field-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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. 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 3 institutions in 2 countries.

Izadora Volpato RossiGraduate Program in Cell and Molecular Biology, Federal University of Paraná, Curitiba, PR, Brazil.
Maria Alice Ferreira NunesGraduate Program in Cell and Molecular Biology, Federal University of Paraná, Curitiba, PR, Brazil.
Bruna SabatkeCarlos Chagas Institute, Fundação Oswaldo Cruz (FIOCRUZ-PR), Curitiba, PR, Brazil.
Hennrique Taborda RibasGraduate Program in Biochemistry Sciences, Federal University of Paraná, Curitiba, PR, Brazil.
Sheila Maria Brochado WinnischoferGraduate Program in Biochemistry Sciences, Federal University of Paraná, Curitiba, PR, Brazil.
Augusto Savio Peixoto RamosCarlos Chagas Institute, Fundação Oswaldo Cruz (FIOCRUZ-PR), Curitiba, PR, Brazil.
Jameel Malhador InalSchool of Human Sciences, London Metropolitan University, London, United Kingdom.
Marcel Ivan RamirezCarlos Chagas Institute, Fundação Oswaldo Cruz (FIOCRUZ-PR), Curitiba, PR, Brazil.
Fundação Oswaldo Cruz · BRUniversidade Federal do Paraná · BRUniversity of Hertfordshire · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Chagas disease is a neglected tropical disease caused by Methods: Here, we have selected a population of epimastigotes (a replicative form) from Results: The 2R population had a favored metacyclogenesis compared with wild-type (WT) parasites. 2R metacyclic trypomastigotes had a two-fold increase in resistance to complementmediated lysis and were at least three times more infective to eukaryotic cells, probably due to a higher GP82 expression in the resistant population. Moreover, we have shown that EVs from resistant parasites can transfer the invasive phenotype to the WT population. In addition, we showed that the virulence phenotype of the selected population remains in the trypomastigote form derived from cell culture, which is more infective and also has a higher rate of release of trypomastigotes from infected cells. Conclusions: Altogether, these data indicate that it is possible to select parasites after exposure to a particular stress factor and that the phenotype of epimastigotes remained in the infective stage. Importantly, EVs seem to be an important virulence fator increasing mechanism in this context of survival and persistence in the host.

Indexed as

Chagas DiseaseExtracellular VesiclesTrypanosoma cruziAnimalsCell DifferentiationComplement System ProteinsHumansMammalsPhenotypeProtozoan ProteinsComplement System ProteinsProtozoan ProteinsChagas diseasecomplement systemextracellular vesiclesinfectionTrypanosoma cruzi

Identifiers

PMID36590580
PMCPMC9795005
OpenAlexW4311479598

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.