Evidence map›Paper›PMID 14638766›Full record

ArticleInfection and immunity2003

Porphyromonas gingivalis lipopolysaccharide antagonizes Escherichia coli lipopolysaccharide at toll-like receptor 4 in human endothelial cells.

Stephen R Coats, Robert A Reife, Brian W Bainbridge, T Thu-Thao Pham, Richard P Darveau

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 138 citations in OpenAlex.

  1. Trial
  2. Article
  3. Noradrenaline Synergistically EnhancesInternational journal of molecular sciences · 2025
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  4. Article
  5. Role of DDR1 in Regulating MMPs in External Root Resorption.International journal of molecular sciences · 2024
    Article
  6. Article
  7. Article
  8. Lipopolysaccharide fromInternational journal of molecular sciences · 2022
    Article
  9. Review
  10. Article
  11. Pathogenesis of Important Virulence Factors ofFrontiers in cellular and infection microbiology · 2019
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. [Correlation between pathogen-associated molecular patterns and periodontitis].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2016
    Article
  17. Article
  18. Review
  19. The role of the local microbial ecosystem in respiratory health and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Review
  20. 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

5 authors at 1 institution in 1 country.

Stephen R CoatsDepartment of Periodontics, University of Washington, Seattle, Washington 98195, USA. scoats@u.washington.edu
Robert A Reife
Brian W Bainbridge
T Thu-Thao Pham
Richard P Darveau
University of Washington · US

Funding

P. GINGIVALIS LPS-MODULATION OF INNATE HOST DEFENSER01DE012768 · NIDCR · UNIVERSITY OF WASHINGTON · PI DARVEAU, RICHARD PETERS · 1999 to 2014
$5.0M
NIDCR NIH HHS R01 DE012768NIDCR NIH HHS R01 DE12768
6 · The paper itself

Abstract

E. coli lipopolysaccharide (LPS) induces cytokine and adhesion molecule expression via the toll-like receptor 4 (TLR4) signaling complex in human endothelial cells. In the present study, we investigated the mechanism by which Porphyromonas gingivalis LPS antagonizes E. coli LPS-dependent activation of human endothelial cells. P. gingivalis LPS at 1 micro g/ml inhibited both E. coli LPS (10 ng/ml) and Mycobacterium tuberculosis heat shock protein (HSP) 60.1 (10 micro g/ml) stimulation of E-selectin mRNA expression in human umbilical vein endothelial cells (HUVEC) without inhibiting interleukin-1 beta (IL-1beta) stimulation. P. gingivalis LPS (1 micro g/ml) also blocked both E. coli LPS-dependent and M. tuberculosis HSP60.1-dependent but not IL-1beta-dependent activation of NF-kappaB in human microvascular endothelial (HMEC-1) cells, consistent with antagonism occurring upstream from the TLR/IL-1 receptor adaptor protein, MyD88. Surprisingly, P. gingivalis LPS weakly but significantly activated NF-kappaB in HMEC-1 cells in the absence of E. coli LPS, and the P. gingivalis LPS-dependent agonism was blocked by transient expression of a dominant negative murine TLR4. Pretreatment of HUVECs with P. gingivalis LPS did not influence the ability of E. coli LPS to stimulate E-selectin mRNA expression. Taken together, these data provide the first evidence that P. gingivalis LPS-dependent antagonism of E. coli LPS in human endothelial cells likely involves the ability of P. gingivalis LPS to directly compete with E. coli LPS at the TLR4 signaling complex.

Indexed as

AntibiosisCells, CulturedEndothelial CellsEscherichia coliHumansLipopolysaccharidesMembrane GlycoproteinsMicrocirculationPorphyromonas gingivalisReceptors, Cell SurfaceSignal TransductionToll-Like Receptor 4Toll-Like ReceptorsUmbilical VeinsLipopolysaccharidesMembrane GlycoproteinsReceptors, Cell SurfaceTLR4 protein, humanToll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID14638766
PMCPMC308937
OpenAlexW2098924752

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.