Evidence map›Paper›PMID 15731036›Full record

ArticleInfection and immunity2005

Functional implication of the hydrolysis of platelet endothelial cell adhesion molecule 1 (CD31) by gingipains of Porphyromonas gingivalis for the pathology of periodontal disease.

Peter L W Yun, Arthur A Decarlo, Cheryl C Chapple, Neil Hunter

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. 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
0.9field-weighted citation impact, top 30% 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, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The impact of periodontitis on vascular endothelial dysfunction.Frontiers in cellular and infection microbiology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. The Effects ofFrontiers in immunology · 2021
    Review
  9. Journal of dental research · 2020
    Article
  10. CD31 is a key coinhibitory receptor in the development of immunogenic dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  11. Article
  12. Review
  13. Review
  14. TCR stimulation drives cleavage and shedding of the ITIM receptor CD31.Journal of immunology (Baltimore, Md. : 1950) · 2010
    Article
  15. Article
  16. Article
  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 2 institutions in 2 countries.

Peter L W YunInstitute of Dental Research, Westmead Millennium Institute and Centre for Oral Health, Westmead Hospital, P.O. Box 533, Wentworthville, Sydney, NSW 2145, Australia. plwyun@yahoo.com
Arthur A Decarlo
Cheryl C Chapple
Neil Hunter
Westmead Institute · AUNova Southeastern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis is a response of highly vascularized tissues to the adjacent microflora of dental plaque. Progressive disease has been related to consortia of anaerobic bacteria, with the gram-negative organism Porphyromonas gingivalis particularly implicated. The gingipains, comprising a group of cysteine proteinases and associated hemagglutinin domains, are major virulence determinants of this organism. As vascular expression of leukocyte adhesion molecules is a critical determinant of tissue response to microbial challenge, the objective of this study was to determine the capacity of gingipains to modulate the expression and function of these receptors. Given the potential multifunctional role of platelet endothelial cell adhesion molecule 1 (PECAM-1) in the vasculature, the effect of gingipains on PECAM-1 expression by endothelial cells was examined. Activated gingipains preferentially down-regulated PECAM-1 expression on endothelial cells compared with vascular cell adhesion molecule 1 and endothelial-leukocyte adhesion molecule 1, but the reduction in PECAM-1 expression was completely inhibited in the presence of the cysteine proteinase inhibitor TLCK (Nalpha-p-tosyl-l-lysine chloromethyl ketone). Endothelial monolayers treated with activated gingipains demonstrated progressive intercellular gap formation that correlated with reduced intercellular junctional PECAM-1 expression as determined by Western blotting and immunofluorescence microscopy. This was accompanied by enhanced transfer of both albumin and neutrophils across the monolayer. The results suggest that degradation of PECAM-1 by gingipains contributes to increased vascular permeability and neutrophil flux at disease sites.

Indexed as

Adhesins, BacterialCell Membrane PermeabilityCells, CulturedCysteine EndopeptidasesEndothelial CellsEndothelium, VascularE-SelectinGingipain Cysteine EndopeptidasesHemagglutininsHumansHydrolysisNeutrophil InfiltrationPeriodontal DiseasesPlatelet Endothelial Cell Adhesion Molecule-1Porphyromonas gingivalisTumor Necrosis Factor-alphaAdhesins, BacterialCysteine EndopeptidasesE-SelectinGingipain Cysteine EndopeptidasesHemagglutininsPlatelet Endothelial Cell Adhesion Molecule-1Tumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID15731036
PMCPMC1064963
OpenAlexW1988092678

What OpenQuestion holds

Textmetadata
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.