Evidence map›Paper›PMID 30251911›Full record

ArticleVirulence2018

Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis.

Yujiro Hirose, Masaya Yamaguchi, Kana Goto, Tomoko Sumitomo, Masanobu Nakata, Shigetada Kawabata

Open access · goldAbstract read
In one paragraph

Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Pneumococcal Encounter With the Blood-Brain Barrier Endothelium.Frontiers in cellular and infection microbiology · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Frontiers in cellular and infection microbiology · 2019
    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

6 authors at 1 institution in 1 country.

Yujiro Hirosea Department of Oral and Molecular Microbiology , Osaka University Graduate School of Dentistry , Suita , Osaka , Japan.ORCID 0000-0001-6338-4767
Masaya Yamaguchia Department of Oral and Molecular Microbiology , Osaka University Graduate School of Dentistry , Suita , Osaka , Japan.
Kana Gotoa Department of Oral and Molecular Microbiology , Osaka University Graduate School of Dentistry , Suita , Osaka , Japan.
Tomoko Sumitomoa Department of Oral and Molecular Microbiology , Osaka University Graduate School of Dentistry , Suita , Osaka , Japan.
Masanobu Nakataa Department of Oral and Molecular Microbiology , Osaka University Graduate School of Dentistry , Suita , Osaka , Japan.
Shigetada Kawabataa Department of Oral and Molecular Microbiology , Osaka University Graduate School of Dentistry , Suita , Osaka , Japan.
The University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Streptococcus pneumoniae is a major pathogen that causes pneumonia, sepsis, and meningitis. The candidate combox site 4 (ccs4) gene has been reported to be a pneumococcal competence-induced gene. Such genes are involved in development of S. pneumoniae competence and virulence, though the functions of ccs4 remain unknown. In the present study, the role of Ccs4 in the pathogenesis of pneumococcal meningitis was examined. We initially constructed a ccs4 deletion mutant and complement strains, then examined their association with and invasion into human brain microvascular endothelial cells. Wild-type and Ccs4-complemented strains exhibited significantly higher rates of association and invasion as compared to the ccs4 mutant strain. Deletion of ccs4 did not change bacterial growth activity or expression of NanA and CbpA, known brain endothelial pneumococcal adhesins. Next, mice were infected either intravenously or intranasally with pneumococcal strains. In the intranasal infection model, survival rates were comparable between wild-type strain-infected and ccs4 mutant strain-infected mice, while the ccs4 mutant strain exhibited a lower level of virulence in the intravenous infection model. In addition, at 24 hours after intravenous infection, the bacterial burden in blood was comparable between the wild-type and ccs4 mutant strain-infected mice, whereas the wild-type strain-infected mice showed a significantly higher bacterial burden in the brain. These results suggest that Ccs4 contributes to pneumococcal invasion of host brain tissues and functions as a virulence factor.

Indexed as

A549 CellsAdhesins, BacterialAnimalsBacterial LoadBacterial ProteinsBrainDisease Models, AnimalEndothelial CellsFemaleHumansMeningitis, PneumococcalMiceMutationStreptococcus pneumoniaeVirulenceVirulence FactorsAdhesins, BacterialBacterial ProteinsVirulence Factorsblood-brain barrierCcs4meningitispathogenesisStreptococcus pneumoniae

Identifiers

PMID30251911
PMCPMC6177246
OpenAlexW2892851341

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.