Evidence map›Paper›PMID 32681704›Full record

ArticleThe FEBS journal2021

Mechanisms of vascular damage by systemic dissemination of the oral pathogen Porphyromonas gingivalis.

Cher Farrugia, Graham P Stafford, Jan Potempa, Robert N Wilkinson, Yan Chen, Craig Murdoch, Magdalena Widziolek

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The FEBS journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 4 countries.

Cher FarrugiaSchool of Clinical Dentistry, University of Sheffield, UK.ORCID 0000-0003-1318-8885
Graham P StaffordSchool of Clinical Dentistry, University of Sheffield, UK.
Jan PotempaDepartment of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland.
Robert N WilkinsonSchool of Life Sciences, Medical School, University of Nottingham, UK.
Yan ChenDepartment of Infection, Immunity and Cardiovascular Disease, Medical School, University of Sheffield, UK.
Craig MurdochSchool of Clinical Dentistry, University of Sheffield, UK.ORCID 0000-0001-9724-122X
Magdalena WidziolekSchool of Clinical Dentistry, University of Sheffield, UK.
University of Sheffield · GBJagiellonian University · PLInstitute of Infection and Immunity · CAUniversity of Nottingham · GB

Funding

Bacterial peptidylarginine deiminase, a link between gums and joint diseaseR01DE022597 · NIDCR · UNIVERSITY OF LOUISVILLE · PI POTEMPA, JAN S · 2013 to 2023
$3.7M
NIDCR NIH HHS R01 DE022597
6 · The paper itself

Abstract

Several studies have shown a clear association between periodontal disease and increased risk of cardiovascular disease. Porphyromonas gingivalis (Pg), a key oral pathogen, and its cell surface-expressed gingipains, induce oedema in a zebrafish larvae infection model although the mechanism of these vascular effects is unknown. Here, we aimed to determine whether Pg-induced vascular damage is mediated by gingipains. In vitro, human endothelial cells from different vascular beds were invaded by wild-type (W83) but not gingipain-deficient (ΔK/R-ab) Pg. W83 infection resulted in increased endothelial permeability as well as decreased cell surface abundance of endothelial adhesion molecules PECAM-1 and VE-cadherin compared to infection with ΔK/R-ab. In agreement, when transgenic zebrafish larvae expressing fluorescently labelled PECAM-1 or VE-cadherin were systemically infected with W83 or ΔK/R-ab, a significant reduction in adhesion molecule fluorescence was observed specifically in endothelium proximal to W83 bacteria through a gingipain-dependent mechanism. Furthermore, this was associated with increased vascular permeability in vivo when assessed by dextran leakage microangiography. These data are the first to show that Pg directly mediates vascular damage in vivo by degrading PECAM-1 and VE-cadherin. Our data provide a molecular mechanism by which Pg might contribute to cardiovascular disease.

Indexed as

AnimalsAnimals, Genetically ModifiedAntigens, CDBacteroidaceae InfectionsCadherin 5CadherinsCapillary PermeabilityCardiomegalyEdemaEmbryo, NonmammalianEndothelial CellsFluorescein AngiographyGene ExpressionGenes, ReporterGingipain Cysteine EndopeptidasesGreen Fluorescent ProteinsAntigens, CDCadherin 5Cadherinsenhanced green fluorescent proteinGingipain Cysteine EndopeptidasesGreen Fluorescent ProteinsPECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1cardiovascular diseaseendothelial cellsgingipainperiodontal diseasePorphyromonas gingivalis

Identifiers

PMID32681704
PMCPMC9994420
OpenAlexW3043145023

What OpenQuestion holds

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LicenceTDM
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.