Evidence map›Paper›PMID 26993626›Full record

ArticleJournal of oral microbiology2016

Major neutrophil functions subverted by Porphyromonas gingivalis.

Ingar Olsen, George Hajishengallis

Open access · goldAbstract read
In one paragraph

Article in Journal of oral microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

50 citing papers in PubMed, 74 citations in OpenAlex.

  1. Trial
  2. Oxidative Stress ReshapesAntibiotics (Basel, Switzerland) · 2026
    Article
  3. Review
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  9. Article
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  15. Article
  16. Article
  17. Metronidazole enhances killing ofFrontiers in oral health · 2022
    Article
  18. Shut-Down of Type IX Protein Secretion Alters the Host Immune Response toFrontiers in cellular and infection microbiology · 2022
    Article
  19. Article
  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

2 authors at 2 institutions in 2 countries.

Ingar OlsenDepartment of Oral Microbiology, Faculty of Dentistry, University of Oslo, Oslo, Norway; ingar.olsen@odont.uio.no.
George HajishengallisDepartment of Microbiology, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.
University of Oslo · NOUniversity of Pennsylvania · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Oral Immunity and Adjuvant ReceptorsR01DE017138 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2006 to 2014
$3.8M
Del-1: Molecular and Cellular Targets in PeriodontitisR01DE024716 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2015 to 2019
$2.0M
Novel mechanisms and 'complement-ary' therapy in periodontitisR01DE021685 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2012 to 2016
$2.0M
NIAID NIH HHS P01 AI068730NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE017138NIDCR NIH HHS R01 DE021685NIDCR NIH HHS R01 DE024716
6 · The paper itself

Abstract

Polymorphonuclear leukocytes (neutrophils) constitute an integrated component of the innate host defense in the gingival sulcus/periodontal pocket. However, the keystone periodontal pathogen Porphyromonas gingivalis has in the course of evolution developed a number of capacities to subvert this defense to its own advantage. The present review describes the major mechanisms that P. gingivalis uses to subvert neutrophil homeostasis, such as impaired recruitment and chemotaxis, resistance to granule-derived antimicrobial agents and to the oxidative burst, inhibition of phagocytic killing while promoting a nutritionally favorable inflammatory response, and delay of neutrophil apoptosis. Studies in animal models have shown that at least some of these mechanisms promote the dysbiotic transformation of the periodontal polymicrobial community, thereby leading to inflammation and bone loss. It is apparent that neutrophil-P. gingivalis interactions and subversion of innate immunity are key contributing factors to the pathogenesis of periodontal disease.

Indexed as

interactionneutrophilsperiodontal homeostasisPorphyromonas gingivalissubversion of immunity

Identifiers

PMID26993626
PMCPMC4799392
OpenAlexW2300803586

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.