Evidence map›Paper›PMID 28759055›Full record

ArticlePloS one2017

A role for the tfs3 ICE-encoded type IV secretion system in pro-inflammatory signalling by the Helicobacter pylori Ser/Thr kinase, CtkA.

Maher N Alandiyjany, Nicola J Croxall, Jane I Grove, Robin M Delahay

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Global diversity of integrating conjugative elements (ICEs) inbioRxiv : the preprint server for biology · 2025
    Article
  2. Article
  3. Implications of lncRNAs inFrontiers in cellular and infection microbiology · 2024
    Review
  4. Study ofCancers · 2023
    Article
  5. Article
  6. Review
  7. Inflammation and Gastric Cancer.Diseases (Basel, Switzerland) · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Integrative and Conjugative Elements ofFrontiers in cellular and infection microbiology · 2020
    Article
  13. Four Chromosomal Type IV Secretion Systems inFrontiers in microbiology · 2020
    Review
  14. Pathogenesis and clinical management ofWorld journal of gastroenterology · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Maher N AlandiyjanyNIHR Nottingham Digestive Diseases Biomedical Research Unit, Nottingham University Hospitals NHS Trust and University of Nottingham, Nottingham, United Kingdom.
Nicola J CroxallNIHR Nottingham Digestive Diseases Biomedical Research Unit, Nottingham University Hospitals NHS Trust and University of Nottingham, Nottingham, United Kingdom.
Jane I GroveNIHR Nottingham Digestive Diseases Biomedical Research Unit, Nottingham University Hospitals NHS Trust and University of Nottingham, Nottingham, United Kingdom.
Robin M DelahayNIHR Nottingham Digestive Diseases Biomedical Research Unit, Nottingham University Hospitals NHS Trust and University of Nottingham, Nottingham, United Kingdom.ORCID http://orcid.org/0000-0002-7108-565X
Nottingham University Hospitals NHS Trust · GB

Funding

Medical Research Council G0901104
6 · The paper itself

Abstract

Two distinct type IV secretion systems (T4SSs) can be identified in certain Helicobacter pylori strains, encoded on mobile genetic elements termed tfs3 and tfs4. Although their function remains unknown, both have been implicated in clinical outcomes of H. pylori infection. Here we provide evidence that the Tfs3 T4SS is required for activity of the pro-inflammatory Ser/Thr kinase protein, CtkA, in a gastric epithelial cell infection model. Previously, purified recombinant CtkA protein has been shown to upregulate NF-kappaB signalling and induce TNF-alpha and IL-8 cytokine secretion from cultured macrophages suggesting that it may potentiate the H. pylori-mediated inflammatory response. In this study, we show that CtkA expressed from its native host, H. pylori has a similar capacity for stimulation of a pro-inflammatory response from gastric epithelial cells. CtkA interaction was found to be dependent upon a complement of tfs3 T4SS genes, but independent of the T4SSs encoded by either tfs4 or the cag pathogenicity island. Moreover, the availability of CtkA for host cell interaction was shown to be conditional upon the carboxyl-terminus of CtkA, encoding a putative conserved secretion signal common to other variably encoded Tfs3 proteins. Collectively, our observations indicate a role for the Tfs3 T4SS in CtkA-mediated pro-inflammatory signalling by H. pylori and identify CtkA as a likely Tfs3 T4SS secretion substrate.

Indexed as

Signal TransductionBacterial ProteinsCell LineCytokinesEpithelial CellsHelicobacter pyloriHumansProtein DomainsProtein Serine-Threonine KinasesType IV Secretion SystemsBacterial ProteinsCtkA protein, Helicobacter pyloriCytokinesProtein Serine-Threonine KinasesType IV Secretion Systems

Identifiers

PMID28759055
PMCPMC5536186
OpenAlexW2739548550

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.