Evidence map›Paper›PMID 27796929›Full record

ArticleJournal of microbiology (Seoul, Korea)2016

Potential for colonization of O111:H25 atypical enteropathogenic E. coli.

Marta O Domingos, Keyde C M Melo, Irys Viana Neves, Cristiane M Mota, Rita C Ruiz, Bruna S Melo, Raphael C Lima, Denise S P Q Horton, Monamaris M Borges, Marcia R Franzolin

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of microbiology (Seoul, Korea), 2016. 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
1.2field-weighted citation impact, top 20% 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, 9 citations in OpenAlex.

  1. 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

10 authors at 1 institution in 1 country.

Marta O DomingosLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil. marta.domingos@butantan.gov.br.
Keyde C M MeloLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Irys Viana NevesLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Cristiane M MotaLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Rita C RuizLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Bruna S MeloLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Raphael C LimaLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Denise S P Q HortonLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Monamaris M BorgesLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Marcia R FranzolinLaboratório de Bacteriologia, Instituto Butantan Av. Vital Brazil, 1500, 05503-900, São Paulo, SP, Brazil.
Instituto Butantan · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Using clonal phylogenetic methods, it has been demonstrated that O111:H25 atypical enteropathogenic E. coli (aEPEC) strains belong to distinct clones, suggesting the possibility that their ability to interact with different hosts and abiotic surfaces can vary from one clone to another. Accordingly, the ability of O111:H25 aEPEC strains derived from human, cat and dogs to adhere to epithelial cells has been investigated, along with their ability to interact with macrophages and to form biofilms on polystyrene, a polymer used to make biomedical devices. The results demonstrated that all the strains analyzed were able to adhere to, and to form pedestals on, epithelial cells, mechanisms used by E. coli to become strongly attached to the host. The strains also show a Localized-Adherence-Like (LAL) pattern of adhesion on HEp-2 cells, a behavior associated with acute infantile diarrhea. In addition, the O111:H25 aEPEC strains derived either from human or domestic animals were able to form long filaments, a phenomenon used by some bacteria to avoid phagocytosis. O111:H25 aEPEC strains were also encountered inside vacuoles, a characteristic described for several bacterial strains as a way of protecting themselves against the environment. They were also able to induce TNF-α release via two routes, one dependent on TLR-4 and the other dependent on binding of Type I fimbriae. These O111:H25 strains were also able to form biofilms on polystyrene. In summary the results suggest that, regardless of their source (i.e. linked to human origin or otherwise), O111:H25 aEPEC strains carry the potential to cause human disease.

Indexed as

Bacterial AdhesionAnimalsBiofilmsCatsDogsEnteropathogenic Escherichia coliEpithelial CellsEscherichia coli InfectionsEscherichia coli ProteinsFimbriae, BacterialHumansMacrophagesMicePhylogenyPolystyrenesToll-Like Receptor 4Escherichia coli ProteinsPolystyrenesTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alphaVirulence FactorsaEPECatypical enteropathogenic Escherichia colibiofilm formationcat and dogsO111:H25 serogroupvirulence factors

Identifiers

PMID27796929
OpenAlexW2544111489

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.