Evidence map›Paper›PMID 29860256›Full record

ArticleJournal of innate immunity2018

Porphyromonas gingivalis Peptidyl Arginine Deiminase Can Modulate Neutrophil Activity via Infection of Human Dental Stem Cells.

Katja Kriebel, Cathleen Hieke, Robby Engelmann, Jan Potempa, Brigitte Müller-Hilke, Hermann Lang, Bernd Kreikemeyer

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Pathogenesis ofFrontiers in cellular and infection microbiology · 2026
    Review
  3. Review
  4. Impact of increasedJournal of oral microbiology · 2025
    Article
  5. Review
  6. Article
  7. International journal of molecular sciences · 2023
    Article
  8. Review
  9. Review
  10. Citrullinome ofMolecular & cellular proteomics : MCP · 2020
    Article
  11. Who is WHO?Journal of innate immunity · 2020
    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

7 authors at 2 institutions in 3 countries.

Katja KriebelDepartment of Operative Dentistry and Periodontology, Rostock University Medical Center, Rostock, Germany.
Cathleen HiekeInstitute<bold></bold> of Medical Microbiology, Virology and Hygiene, Rostock University Medical Center, Rostock, Germany.
Robby EngelmannInstitute of Immunology, Rostock University Medical Center, Rostock, Germany.
Jan PotempaJagiellonian University, Faculty of Biochemistry, Biophysics and Biotechnology, Krakow, Poland.
Brigitte Müller-HilkeInstitute of Immunology, Rostock University Medical Center, Rostock, Germany.
Hermann LangDepartment of Operative Dentistry and Periodontology, Rostock University Medical Center, Rostock, Germany.
Bernd KreikemeyerInstitute<bold></bold> of Medical Microbiology, Virology and Hygiene, Rostock University Medical Center, Rostock, Germany.
University of Rostock · DEJagiellonian University · PL

Funding

Bacterial peptidylarginine deiminase, a link between gums and joint diseaseR01DE022597 · NIDCR · UNIVERSITY OF LOUISVILLE · PI POTEMPA, JAN S · 2013 to 2023
$3.7M
Blocking of IL-6 function to prevent Pg mediated Th17 responseR21DE023207 · NIDCR · UNIVERSITY OF LOUISVILLE · PI POTEMPA, JAN S · 2013 to 2014
$413k
NIDCR NIH HHS R01 DE022597NIDCR NIH HHS R21 DE023207
6 · The paper itself

Abstract

Periodontitis (PD) is a widespread chronic inflammatory disease in the human population. Porphyromonas gingivalis is associated with PD and can citrullinate host proteins via P. gingivalis peptidyl arginine deiminase (PPAD). Here, we hypothesized that infection of human dental follicle stem cells (hDFSCs) with P. gingivalis and subsequent interaction with neutrophils will alter the neutrophil phenotype. To test this hypothesis, we established and analyzed a triple-culture system of neutrophils and hDFSCs primed with P. gingivalis. Mitogen-activated pathway blocking reagents were applied to gain insight into stem cell signaling after infection. Naïve hDFSCs do not influence the neutrophil phenotype. However, infection of hDFSCs with P. gingivalis prolongs the survival of neutrophils and increases their migration. These phenotypic changes depend on direct cellular contacts and PPAD expression by P. gingivalis. Active JNK and ERK pathways in primed hDFSCs are essential for the phenotypic changes in neutrophils. Collectively, our results confirm that P. gingivalis modifies hDFSCs, thereby causing an immune imbalance.

Indexed as

Bacterial ProteinsBacteroidaceae InfectionsCells, CulturedCoculture TechniquesDental SacHumansImmunomodulationMAP Kinase Kinase 4Neutrophil ActivationNeutrophilsPeriodontitisPorphyromonas gingivalisProtein-Arginine DeiminasesSignal TransductionStem CellsBacterial ProteinsMAP Kinase Kinase 4Protein-Arginine DeiminasesBacterial infectionCitrullinationImmune modulationNeutrophilsPeptidyl arginine deiminasePeriodontitisPorphyromonas gingivalisStem cellsViability

Identifiers

PMID29860256
PMCPMC6158109
OpenAlexW2805056896

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.