Evidence map›Paper›PMID 25790373›Full record

ArticlePloS one2015

Disruption of Escherichia coli Nissle 1917 K5 capsule biosynthesis, through loss of distinct kfi genes, modulates interaction with intestinal epithelial cells and impact on cell health.

Jonathan Nzakizwanayo, Sandeep Kumar, Lesley A Ogilvie, Bhavik A Patel, Cinzia Dedi, Wendy M Macfarlane, Brian V Jones

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  7. Review
  8. Advances inMaterials today. Bio · 2023
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  10. Sequestration of gut pathobionts in intraluminal casts, a mechanism to avoid dysregulated T cell activation by pathobionts.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Transcriptional Profiling of the ProbioticInternational journal of molecular sciences · 2020
    Article
  15. Review
  16. Article
  17. 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

7 authors at 2 institutions in 1 country.

Jonathan NzakizwanayoSchool of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, United Kingdom.
Sandeep KumarSchool of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, United Kingdom.
Lesley A OgilvieSchool of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, United Kingdom.
Bhavik A PatelSchool of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, United Kingdom.
Cinzia DediSchool of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, United Kingdom.
Wendy M MacfarlaneSchool of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, United Kingdom.
Brian V JonesSchool of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, United Kingdom; Queen Victoria Hospital NHS Foundation Trust, East Grinstead, West Sussex, United Kingdom.
University of Brighton · GBQueen Victoria Hospital NHS Foundation Trust · GB

Funding

Medical Research Council G0901553
6 · The paper itself

Abstract

Escherichia coli Nissle 1917 (EcN) is among the best characterised probiotics, with a proven clinical impact in a range of conditions. Despite this, the mechanisms underlying these "probiotic effects" are not clearly defined. Here we applied random transposon mutagenesis to identify genes relevant to the interaction of EcN with intestinal epithelial cells. This demonstrated mutants disrupted in the kfiB gene, of the K5 capsule biosynthesis cluster, to be significantly enhanced in attachment to Caco-2 cells. However, this phenotype was distinct from that previously reported for EcN K5 deficient mutants (kfiC null mutants), prompting us to explore further the role of kfiB in EcN:Caco-2 interaction. Isogenic mutants with deletions in kfiB (EcNΔkfiB), or the more extensively characterised K5 capsule biosynthesis gene kfiC (EcNΔkfiC), were both shown to be capsule deficient, but displayed divergent phenotypes with regard to impact on Caco-2 cells. Compared with EcNΔkfiC and the EcN wild-type, EcNΔkfiB exhibited significantly greater attachment to Caco-2 cells, as well as apoptotic and cytotoxic effects. In contrast, EcNΔkfiC was comparable to the wild-type in these assays, but was shown to induce significantly greater COX-2 expression in Caco-2 cells. Distinct differences were also apparent in the pervading cell morphology and cellular aggregation between mutants. Overall, these observations reinforce the importance of the EcN K5 capsule in host-EcN interactions, but demonstrate that loss of distinct genes in the K5 pathway can modulate the impact of EcN on epithelial cell health.

Indexed as

Bacterial AdhesionBacterial CapsulesCaco-2 CellsCyclooxygenase 2Epithelial CellsEscherichia coliEscherichia coli ProteinsGlycosyltransferasesHumansIntestinesMutagenesis, Insertionalcapsular polysaccharide K5Cyclooxygenase 2Escherichia coli ProteinsGlycosyltransferasesKfiC protein, E coliPTGS2 protein, human

Identifiers

PMID25790373
PMCPMC4366286
OpenAlexW2058864644

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LicenceCC BY
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Registered trials

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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.