Evidence map›Paper›PMID 30954574›Full record

ArticleJournal of molecular biology2019

Role of Phenol-Soluble Modulins in Staphylococcus epidermidis Biofilm Formation and Infection of Indwelling Medical Devices.

Katherine Y Le, Amer E Villaruz, Yue Zheng, Lei He, Emilie L Fisher, Thuan H Nguyen, Trung V Ho, Anthony J Yeh, Hwang-Soo Joo, Gordon Y C Cheung and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 72 citations in OpenAlex.

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  20. Antimicrobial Treatment ofAntibiotics (Basel, Switzerland) · 2023
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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

11 authors at 2 institutions in 2 countries.

Katherine Y LePathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA; Division of Hospital Internal Medicine, Department of Medicine, Mayo Clinic College of Medicine, 200 1st Street SW, Rochester, MN 55902, USA.
Amer E VillaruzPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Yue ZhengPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Lei HePathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA; Department of Laboratory Medicine, Renji Hospital, School of Medicine, Shanghai Jiaotong University, No. 160 Pujian Road, Shanghai 200127, China.
Emilie L FisherPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Thuan H NguyenPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Trung V HoPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Anthony J YehPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Hwang-Soo JooPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Gordon Y C CheungPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA.
Michael OttoPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, 50 South Drive, Bethesda, MD 20814, USA. Electronic address: motto@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Staphylococcal pathogenesisZIAAI000904 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI OTTO, MICHAEL · 2009 to 2025
$22.6M
Role of the human microbiota and probioticsZIAAI001080 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI OTTO, MICHAEL · 2009 to 2025
$9.7M
Staphylococcus Epidermidis Biofilm FormationZ01AI000904 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI OTTO, MICHAEL J · 2002 to 2008
$2.5M
Intramural NIH HHS Z01 AI000904Intramural NIH HHS ZIA AI000904
6 · The paper itself

Abstract

Phenol-soluble modulins (PSMs) are amphipathic, alpha-helical peptides that are secreted by staphylococci in high amounts in a quorum-sensing-controlled fashion. Studies performed predominantly in Staphylococcus aureus showed that PSMs structure biofilms, which results in reduced biofilm mass, while it has also been reported that S. aureus PSMs stabilize biofilms due to amyloid formation. We here analyzed the roles of PSMs in in vitro and in vivo biofilms of Staphylococcus epidermidis, the leading cause of indwelling device-associated biofilm infection. We produced isogenic deletion mutants for every S. epidermidis psm locus and a sequential deletion mutant in which production of all PSMs was abolished. In vitro analysis substantiated the role of all PSMs in biofilm structuring. PSM-dependent biofilm expansion was not observed, in accordance with our finding that no S. epidermidis PSM produced amyloids. In a mouse model of indwelling device-associated infection, the total psm deletion mutant had a significant defect in dissemination. Notably, the total psm mutant produced a significantly more substantial biofilm on the implanted catheter than the wild-type strain. Our study, which for the first time directly quantified the impact of PSMs on biofilm expansion on an implanted device, shows that the in vivo biofilm infection phenotype in S. epidermidis is in accordance with the PSM biofilm structuring and detachment model, which has important implications for the potential therapeutic application of quorum-sensing blockers.

Indexed as

AnimalsBacterial ToxinsBiofilmsCatheter-Related InfectionsCatheters, IndwellingColony Count, MicrobialDisease Models, AnimalHumansMiceSequence DeletionStaphylococcal InfectionsStaphylococcus epidermidisBacterial Toxinsstaphylococcal delta toxinamyloidscyclophosphamidedevice-associated infectionneutrophilsquorum sensing

Identifiers

PMID30954574
PMCPMC10999989
OpenAlexW2932200774

What OpenQuestion holds

Textmetadata
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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.