Evidence map›Paper›PMID 20331800›Full record

ArticleMolecular oral microbiology2010

DNA from Porphyromonas gingivalis and Tannerella forsythia induce cytokine production in human monocytic cell lines.

S E Sahingur, X-J Xia, S Alamgir, K Honma, A Sharma, H A Schenkein

Open access · greenAbstract read
In one paragraph

Article in Molecular oral microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  7. Article
  8. Review
  9. Review
  10. Systemic and Extraradicular Bacterial Translocation in Apical Periodontitis.Frontiers in cellular and infection microbiology · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Relationship of clinical and microbiological variables in patients with type 1 diabetes mellitus and periodontitis.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  20. Novel inflammatory pathways in periodontitis.Advances in dental research · 2014
    Review
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

6 authors at 2 institutions in 1 country.

S E SahingurVirginia Commonwealth University, School of Dentistry, Department of Periodontics, Richmond, VA, USA. ssahingur@vcu.edu
X-J Xia
S Alamgir
K Honma
A Sharma
H A Schenkein
Virginia Commonwealth University · USUniversity at Buffalo, State University of New York · US

Funding

T. forsythia TLR2 ligands and surface glycans coordinate periodontal inflammationR01DE014749 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SHARMA, ASHU · 2003 to 2018
$4.9M
Antiphospholipids in periodontitisR01DE018125 · NIDCR · VIRGINIA COMMONWEALTH UNIVERSITY · PI SCHENKEIN, HARVEY ALLEN · 2008 to 2020
$3.3M
NIDCR NIH HHS DE014749NIDCR NIH HHS DE018125NIDCR NIH HHS R01 DE014749NIDCR NIH HHS R01 DE018125
6 · The paper itself

Abstract

Toll-like receptor 9 (TLR9) expression is increased in periodontally diseased tissues compared with healthy sites indicating a possible role of TLR9 and its ligand, bacterial DNA (bDNA), in periodontal disease pathology. Here, we determine the immunostimulatory effects of periodontal bDNA in human monocytic cells (THP-1). THP-1 cells were stimulated with DNA of two putative periodontal pathogens: Porphyromonas gingivalis and Tannerella forsythia. The role of TLR9 in periodontal bDNA-initiated cytokine production was determined either by blocking TLR9 signaling in THP-1 cells with chloroquine or by measuring IL-8 production and nuclear factor-kappaB (NF-kappaB) activation in HEK293 cells stably transfected with human TLR9. Cytokine production (IL-1beta, IL-6, and TNF-alpha) was increased significantly in bDNA-stimulated cells compared with controls. Chloroquine treatment of THP-1 cells decreased cytokine production, suggesting that TLR9-mediated signaling pathways are operant in the recognition of DNA from periodontal pathogens. Compared with native HEK293 cells, TLR9-transfected cells demonstrated significantly increased IL-8 production (P < 0.001) and NF-kappaB activation in response to bDNA, further confirming the role of TLR9 in periodontal bDNA recognition. The results of PCR arrays demonstrated upregulation of proinflammatory cytokine and NF-kappaB genes in response to periodontal bDNA in THP-1 cells, suggesting that cytokine induction is through NF-kappaB activation. Hence, immune responses triggered by periodontal bacterial nucleic acids may contribute to periodontal disease pathology by inducing proinflammatory cytokine production through the TLR9 signaling pathway.

Indexed as

BacteroidesCell Line, TumorCytokinesDNA, BacterialGene Expression ProfilingHumansInflammation MediatorsInterleukin-1betaInterleukin-6KidneyMonocytesNF-kappa BPorphyromonas gingivalisSignal TransductionToll-Like Receptor 9TransfectionCytokinesDNA, BacterialInflammation MediatorsInterleukin-1betaInterleukin-6NF-kappa BToll-Like Receptor 9Tumor Necrosis Factor-alpha

Identifiers

PMID20331800
PMCPMC4017325
OpenAlexW2073801423

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.