Evidence map›Paper›PMID 26252403›Full record

ReviewPeriodontology 20002015

The inflammasome and danger molecule signaling: at the crossroads of inflammation and pathogen persistence in the oral cavity.

Özlem Yilmaz, Kyu Lim Lee

Open access · bronzeAbstract readReview
In one paragraph

Review in Periodontology 2000, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-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.

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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Pathogens (Basel, Switzerland) · 2022
    Article
  9. Review
  10. Inflammasome Activation in Gingival Epithelial Cells.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. TLR2 and the NLRP3 inflammasome mediate IL-1β production inInternational journal of medical sciences · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. HJournal of oral microbiology · 2019
    Article
  20. A Allele ofOpen life sciences · 2019
    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

2 authors at 1 institution in 1 country.

Özlem Yilmaz
Kyu Lim Lee
University of Florida · US

Funding

Modulation of epithelial cell response by P. gingivalisR01DE016593 · NIDCR · UNIVERSITY OF FLORIDA · PI YILMAZ, OZLEM · 2006 to 2016
$3.3M
The Inflammasome in Gingival Epithelial Cells During Porphyromonas InfectionR01DE019444 · NIDCR · UNIVERSITY OF CALIFORNIA, MERCED · PI OJCIUS, DAVID MARCELO · 2009 to 2012
$1.3M
Modulation of Epithelial Cell Response by P. gingivalisR56DE016593 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI YILMAZ, OZLEM · 2019 to 2019
$355k
NIDCR NIH HHS R01 DE016593NIDCR NIH HHS R01DE016593NIDCR NIH HHS R01 DE019444NIDCR NIH HHS R01DE019444NIDCR NIH HHS R56 DE016593
6 · The paper itself

Abstract

Inflammasomes are an oligomeric assembly of multiprotein complexes that activate the caspase-1-dependent maturation and the subsequent secretion of inflammatory interleukin-1beta and interleukin-18 cytokines in response to a 'danger signal' in vertebrates. The assessment of their significance continues to grow rapidly as the complex biology of various chronic inflammatory conditions is better dissected. Increasing evidence strongly links inflammasomes and host-derived small 'danger molecule ATP' signaling with the modulation of the host immune response by microbial colonizers as well as with potential altering of the microbiome structure and intermicrobial interactions in the host. All of these factors eventually lead to the destructive chronic inflammatory disease state. In the oral cavity, a highly dynamic and multifaceted interplay takes place between the signaling of endogenous danger molecules and colonizing microbes on the mucosal surfaces. This interaction may redirect the local microenvironment to favor the conversion of the resident microbiome toward pathogenicity. This review outlines the major components of the known inflammasome complexes/mechanisms and highlights their regulation, in particular, by oral microorganisms, in relation to periodontal disease pathology. Better characterization of the cellular and molecular biology of the inflammasome will probably identify important potential therapeutic targets for the treatment and prevention of periodontal disease, as well as for other debilitating chronic diseases.

Indexed as

Adenosine TriphosphateAnimalsChronic DiseaseHost-Pathogen InteractionsHumansImmunity, InnateInflammasomesInflammationMouthNLR Family, Pyrin Domain-Containing 3 ProteinPeriodontal DiseasesSignal TransductionAdenosine TriphosphateInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID26252403
PMCPMC4530468
OpenAlexW1959629648

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.