Evidence map›Paper›PMID 30066727›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2018

Intestinal cell migration damage induced by enteropathogenic Escherichia coli strains.

P A Cavalcante, M M G Prata, P H Q S Medeiros, A V Alves da Silva, J S Quetz, M A V Reyes, T S Rodrigues, A K S Santos, S A Ribeiro, H N Veras and 6 more

Open access · goldAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. 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

16 authors at 1 institution in 1 country.

P A CavalcanteDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
M M G PrataDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
P H Q S MedeirosDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
A V Alves da SilvaDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
J S QuetzDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
M A V ReyesDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
T S RodriguesDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
A K S SantosDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
S A RibeiroDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
H N VerasDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
M D BonaDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
M S M G AmaralDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
F A P RodriguesDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
I F N LimaDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
A HavtDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
A A M LimaDepartamento de Fisiologia e Farmacologia, Faculdade de Medicina, Instituto de Biomedicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
Universidade Federal do Ceará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial cell migration is an essential response to enteric pathogens such as enteropathogenic Escherichia coli (EPEC). This study aimed to investigate the effects of EPEC infection on intestinal epithelial cell migration in vitro, as well as the involvement of type III secretion system (T3SS) and Rho GTPases. Crypt intestinal epithelial cells (IEC-6) were infected with EPEC strains (E2348/69, ΔescF, and the LDI001 strain isolated from a malnourished Brazilian child) and commensal E. coli HS. Wound migration and cell death assays were performed at different time-points. Transcription and expression of Rho GTPases were evaluated using real-time PCR and western blotting. Overall, EPEC E2348/69 reduced migration and increased apoptosis and necrosis levels compared to EPEC LDI001 and E. coli HS strains. Moreover, EPEC LDI001 impaired cell migration at a higher level than E. coli HS and increased necrosis after 24 hours compared to the control group. The different profiles of virulence genes between the two wild-type EPEC strains, characterized by the absence of espL and nleE genes in the LDI001, might explain the phenotypic results, playing significant roles on cell migration impairment and cell death-related events. Moreover, the type III secretion system is determinant for the inhibition of intestinal epithelial cell migration by EPEC 2348/69, as its deletion prevented the effect. Active Rac1 concentrations were increased in E2348/69 and LDI001-infected cells, while the T3SS-deficient strain did not demonstrate this activation. This study contributes with valuable insight to characterize the mechanisms involved in the impairment of intestinal cell migration induced by EPEC.

Indexed as

ApoptosisBlotting, WesternCell MovementEnteropathogenic Escherichia coliEpithelial CellsFlow CytometryHumansReal-Time Polymerase Chain Reactionrho GTP-Binding ProteinsType III Secretion SystemsVirulence Factorsrho GTP-Binding ProteinsType III Secretion SystemsVirulence Factors

Identifiers

PMID30066727
PMCPMC6065879
OpenAlexW2884058964

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.