Evidence map›Paper›PMID 19552698›Full record

ArticleCellular microbiology2009

Human Toll-like receptor 4 responses to P. gingivalis are regulated by lipid A 1- and 4'-phosphatase activities.

Stephen R Coats, Jace W Jones, Christopher T Do, Pamela H Braham, Brian W Bainbridge, Thao T To, David R Goodlett, Robert K Ernst, Richard P Darveau

Abstract read
In one paragraph

Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

122 citing papers in PubMed, 168 citations in OpenAlex.

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  10. Macrophage pyroptosis in atherosclerosis: therapeutic potential.Acta biochimica et biophysica Sinica · 2025
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  12. Recognition ofJournal of oral microbiology · 2025
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  13. Oral Microbiome Dysbiosis and Citrullination in Rheumatoid Arthritis.Advances in experimental medicine and biology · 2025
    Review
  14. TheJournal of oral microbiology · 2025
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  15. Article
  16. Journal of oral microbiology · 2025
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  17. Review
  18. Review
  19. The multifaceted role of c-di-AMP signaling in the regulation ofFrontiers in cellular and infection microbiology · 2024
    Article
  20. Article

62 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Stephen R CoatsDepartment of Periodontics, School of Dentistry, University of Washington, 1959 NE Pacific St., Seattle, WA 98195-7444, USA. scoats@u.washington.edu
Jace W Jones
Christopher T Do
Pamela H Braham
Brian W Bainbridge
Thao T To
David R Goodlett
Robert K Ernst
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 DE12768NIDCR NIH HHS R01 DE012768
6 · The paper itself

Abstract

Signal transduction following binding of lipopolysaccharide (LPS) to Toll-like receptor 4 (TLR4) is an essential aspect of host innate immune responses to infection by Gram-negative pathogens. Here, we describe a novel molecular mechanism used by a prevalent human bacterial pathogen to evade and subvert the human innate immune system. We show that the oral pathogen, Porphyromonas gingivalis, uses endogenous lipid A 1- and 4'-phosphatase activities to modify its LPS, creating immunologically silent, non-phosphorylated lipid A. This unique lipid A provides a highly effective mechanism employed by this bacterium to evade TLR4 sensing and to resist killing by cationic antimicrobial peptides. In addition, lipid A 1-phosphatase activity is suppressed by haemin, an important nutrient in the oral cavity. Specifically, P. gingivalis grown in the presence of high haemin produces lipid A that acts as a potent TLR4 antagonist. These results suggest that haemin-dependent regulation of lipid A 1-dephosphorylation can shift P. gingivalis lipid A activity from TLR4 evasive to TLR4 suppressive, potentially altering critical interactions between this bacterium, the local microbial community and the host innate immune system.

Indexed as

Bacterial ProteinsColony Count, MicrobialEnzyme InhibitorsHeminHumansLipid AMicrobial ViabilityModels, BiologicalNF-kappa BPhosphoric Monoester HydrolasesPorphyromonas gingivalisSignal TransductionToll-Like Receptor 4Virulence FactorsBacterial ProteinsEnzyme InhibitorsHeminLipid Alipid A 1-phosphatase, Porphyromonas gingivalislipid A 4'-phosphataseNF-kappa BPhosphoric Monoester HydrolasesTLR4 protein, humanToll-Like Receptor 4Virulence Factors

Identifiers

PMID19552698
PMCPMC3074576
OpenAlexW2035337730

What OpenQuestion holds

Textmetadata
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.