Evidence map›Paper›PMID 18395849›Full record

ArticleEuropean journal of immunology2008

TLR4 and S1P receptors cooperate to enhance inflammatory cytokine production in human gingival epithelial cells.

Mehmet A Eskan, Beate G Rose, Manjunatha R Benakanakere, Qun Zeng, Daisuke Fujioka, Michael H Martin, Menq-Jer Lee, Denis F Kinane

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. An Emerging Syndemic of Smoking and Cardiopulmonary Diseases in People Living with HIV in Africa.International journal of environmental research and public health · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Pro-Inflammatory Role of S1PBiomolecules & therapeutics · 2019
    Article
  8. Article
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  10. Article
  11. Review
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  14. Review
  15. Review
  16. Article
  17. GAS6 is a key homeostatic immunological regulator of host-commensal interactions in the oral mucosa.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Article
  19. Article
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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

8 authors at 1 institution in 1 country.

Mehmet A EskanCenter for Oral Health and Systemic Disease, University of Louisville School of Dentistry, University of Louisville, Louisville,KY 40202, USA.
Beate G Rose
Manjunatha R Benakanakere
Qun Zeng
Daisuke Fujioka
Michael H Martin
Menq-Jer Lee
Denis F Kinane
University of Louisville · US

Funding

Epithelial Cell TLRs in Disease SusceptibilityR01DE017384 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI KINANE, DENIS F · 2007 to 2011
$1.7M
NIDCR NIH HHS DE017384NIDCR NIH HHS R01 DE017384
6 · The paper itself

Abstract

Toll-like receptors (TLR) are pattern recognition receptors for highly conserved microbial molecular patterns. Activation of TLR is a pivotal step in the initiation of innate, inflammatory, and immune defense mechanisms. Recent findings indicate that G protein-coupled receptors (GPCR) may modulate TLR signaling, but it is unclear which GPCR are involved in this process. One such cooperation between GPCR and TLR can be attributed to the sphingosine 1-phosphate (S1P) receptor family. The S1P receptors (S1P1-5) are a family of GPCR with a high affinity for S1P, a serum-borne bioactive lipid associated with diverse biological activities such as inflammation and healing. In this study, we show that pro-inflammatory cytokine production, including IL-6 and IL-8, was increased with LPS and concomitant S1P stimulation. Furthermore, elevated cytokine production following LPS and S1P challenge in human gingival epithelial cells (HGEC) was significantly reduced when TLR4, S1P1 or S1P3 signaling was blocked. Our study also shows that S1P1 and S1P3 expression was induced by LPS in HGEC, and this elevated expression enhanced the influence of S1P in its cooperation with TLR4 to increase cytokine production. This cooperation between TLR4 and S1P1 or S1P3 demonstrates that TLR4 and GPCR can interact to enhance cytokine production in epithelial cells.

Indexed as

Cells, CulturedCytokinesEnzyme ActivationEpithelial CellsGingivaHumansLipopolysaccharidesLysophospholipidsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, LysosphingolipidSignal TransductionSphingosineToll-Like Receptor 4Up-RegulationCytokinesLipopolysaccharidesLysophospholipidsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, LysosphingolipidSphingosinesphingosine 1-phosphateToll-Like Receptor 4

Identifiers

PMID18395849
PMCPMC2738989
OpenAlexW1968631247

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.