Evidence map›Paper›PMID 19454663›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Induction of distinct TLR2-mediated proinflammatory and proadhesive signaling pathways in response to Porphyromonas gingivalis fimbriae.

George Hajishengallis, Min Wang, Shuang Liang

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05657015 (Lepidium Sativum Extract Versus Simvastatin as an Adjunctive Local Delivery Agents to Non-Surgical Periodontal Therapy), which is not on this map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.3field-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.

NCT05657015 phase4completednot on this mapstarted 2021, after this paper: background citation

Lepidium Sativum Extract Versus Simvastatin as an Adjunctive Local Delivery Agents to Non-Surgical Periodontal Therapy: A Randomized Controlled Clinical Trial With Biochemical Analysis

TypeinterventionalSponsorAin Shams UniversityRan2021 to 2022Enrolled30ConditionsPeriodontitisArmsLepidium Sativum, Simvastatin
3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Review
  3. Macrophage activation and invasion byJournal of oral microbiology · 2026
    Article
  4. Review
  5. Polymorphic Variants of Peptidylarginine Deiminase Gene fromInternational journal of molecular sciences · 2025
    Article
  6. Article
  7. Review
  8. hTERT Peptide Fragment GV1001 Prevents the Development ofInternational journal of molecular sciences · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Topical application ofInternational journal of molecular medicine · 2022
    Article
  15. TLR2 Activation byFrontiers in immunology · 2022
    Article
  16. Article
  17. The Japanese dental science review · 2021
    Review
  18. Review
  19. 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

3 authors at 2 institutions in 1 country.

George HajishengallisDepartment of Periodontics/Oral Health and Systemic Disease, University of Louisville Health Sciences Center, Louisville, KY 40292, USA.
Min Wang
Shuang Liang
Aurora Periodontics and Implant Dentistry · USUniversity of Louisville · US

Funding

P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Oral Pathogen Exploitation of Innate Recognition as a Function of AgeR01DE018292 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2007 to 2011
$1.6M
NIDCR NIH HHS DE015254NIDCR NIH HHS DE018292NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE018292
6 · The paper itself

Abstract

The oral pathogen Porphyromonas gingivalis, as well as its purified fimbriae, are known to activate TLR2 and induce proinflammatory and proadhesive effects. The TLR2 proinflammatory pathway induces NF-kappaB-dependent inflammatory cytokines, whereas the TLR2 proadhesive pathway is characterized by inside-out signaling that transactivates beta(2) integrin adhesive activities. In this article, using dominant-negative or pharmacological approaches, we show that the two pathways bifurcate and proceed independently downstream of TLR2. Whereas the proinflammatory pathway is dependent on the adaptor molecules Toll/IL-1 receptor domain-containing adaptor protein (also known as Mal) and MyD88, the proadhesive pathway is Toll/IL-1 receptor domain-containing adaptor protein/MyD88-independent and proceeds through PI3K-mediated signaling. Although the Ser/Thr kinase Akt is a major downstream target of PI3K and was activated by P. gingivalis fimbriae in a TLR2- and PI3K-dependent way, Akt was shown not to play a role in the proadhesive pathway. In contrast, another PI3K downstream target, cytohesin-1, was shown to mediate P. gingivalis fimbria-induced activation of beta(2) integrin for ICAM-1 binding. Therefore, P. gingivalis fimbriae activate two distinct TLR2 pathways mediating proinflammatory or proadhesive effects. The delineation of these signaling pathways may provide appropriate targets for selectively inhibiting or enhancing specific activities, depending on whether they undermine or promote the host defense.

Indexed as

Bacterial AdhesionInflammationSignal TransductionCell LineFimbriae, BacterialHumansMembrane GlycoproteinsMyeloid Differentiation Factor 88Phosphatidylinositol 3-KinasesPorphyromonas gingivalisReceptors, Interleukin-1Toll-Like Receptor 2Transcriptional ActivationMembrane GlycoproteinsMYD88 protein, humanMyeloid Differentiation Factor 88Phosphatidylinositol 3-KinasesReceptors, Interleukin-1TIRAP protein, humanToll-Like Receptor 2

Identifiers

PMID19454663
PMCPMC2685460
OpenAlexW1569382726

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.