Evidence map›Paper›PMID 25084357›Full record

ArticlePloS one2014

Cell wall-anchored nuclease of Streptococcus sanguinis contributes to escape from neutrophil extracellular trap-mediated bacteriocidal activity.

Chisato Morita, Ryuichi Sumioka, Masanobu Nakata, Nobuo Okahashi, Satoshi Wada, Takashi Yamashiro, Mikako Hayashi, Shigeyuki Hamada, Tomoko Sumitomo, Shigetada Kawabata

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

36 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Screening of Surface-Exposed Lipoproteins ofFrontiers in microbiology · 2022
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  11. Review
  12. Frontiers in cellular and infection microbiology · 2020
    Article
  13. Article
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  15. Article
  16. Article
  17. Article
  18. Genetics ofMicrobiology spectrum · 2019
    Article
  19. Article
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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.

Chisato MoritaDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Osaka, Japan; Department of Orthodontics and Dentofacial Orthopedics, Osaka University Graduate School of Dentistry, Osaka, Japan.
Ryuichi SumiokaDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Osaka, Japan; Department of Restorative Dentistry and Endodontology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Masanobu NakataDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Nobuo OkahashiDepartment of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Satoshi WadaDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Takashi YamashiroDepartment of Orthodontics and Dentofacial Orthopedics, Osaka University Graduate School of Dentistry, Osaka, Japan.
Mikako HayashiDepartment of Restorative Dentistry and Endodontology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Shigeyuki HamadaResearch Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Tomoko SumitomoDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Shigetada KawabataDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Streptococcus sanguinis, a member of the commensal mitis group of streptococci, is a primary colonizer of the tooth surface, and has been implicated in infectious complications including bacteremia and infective endocarditis. During disease progression, S. sanguinis may utilize various cell surface molecules to evade the host immune system to survive in blood. In the present study, we discovered a novel cell surface nuclease with a cell-wall anchor domain, termed SWAN (streptococcal wall-anchored nuclease), and investigated its contribution to bacterial resistance against the bacteriocidal activity of neutrophil extracellular traps (NETs). Recombinant SWAN protein (rSWAN) digested multiple forms of DNA including NET DNA and human RNA, which required both Mg(2+) and Ca(2+) for optimum activity. Furthermore, DNase activity of S. sanguinis was detected around growing colonies on agar plates containing DNA. In-frame deletion of the swan gene mostly reduced that activity. These findings indicated that SWAN is a major nuclease displayed on the surface, which was further confirmed by immuno-detection of SWAN in the cell wall fraction. The sensitivity of S. sanguinis to NET killing was reduced by swan gene deletion. Moreover, heterologous expression of the swan gene rendered a Lactococcus lactis strain more resistant to NET killing. Our results suggest that the SWAN nuclease on the bacterial surface contributes to survival in the potential situation of S. sanguinis encountering NETs during the course of disease progression.

Indexed as

Cell WallDNA, ViralEnzyme ActivationExtracellular SpaceExtracellular TrapsGene OrderGenetic LociHumansHydrolysisMicrococcal NucleaseNeutrophilsProtein TransportRecombinant Fusion ProteinsRNA, ViralStreptococcus sanguisDNA, ViralMicrococcal NucleaseRecombinant Fusion ProteinsRNA, Viral

Identifiers

PMID25084357
PMCPMC4118848
OpenAlexW1980473800

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Read underepoch 390

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.