Evidence map›Paper›PMID 33377284›Full record

ArticleClinical and experimental dental research2021

Immunological response of human leucocytes after exposure to lipopolysaccharides from Porphyromonas gingivalis.

Sara Alizadehgharib, Anna-Karin Östberg, Agnes Dahlstrand Rudin, Ulf Dahlgren, Karin Christenson

Open access · goldAbstract read
In one paragraph

Article in Clinical and experimental dental research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Oral microbiota in human systematic diseases.International journal of oral science · 2022
    Review
  3. 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

5 authors at 1 institution in 1 country.

Sara AlizadehgharibDepartment of Oral Microbiology and Immunology, University of Gothenburg, The Sahlgrenska Academy, Institute of Odontology, Gothenburg, Sweden.ORCID 0000-0003-1587-9508
Anna-Karin ÖstbergDepartment of Oral Microbiology and Immunology, University of Gothenburg, The Sahlgrenska Academy, Institute of Odontology, Gothenburg, Sweden.
Agnes Dahlstrand RudinDepartment of Oral Microbiology and Immunology, University of Gothenburg, The Sahlgrenska Academy, Institute of Odontology, Gothenburg, Sweden.
Ulf DahlgrenDepartment of Oral Microbiology and Immunology, University of Gothenburg, The Sahlgrenska Academy, Institute of Odontology, Gothenburg, Sweden.
Karin ChristensonDepartment of Oral Microbiology and Immunology, University of Gothenburg, The Sahlgrenska Academy, Institute of Odontology, Gothenburg, Sweden.
University of Gothenburg · SE

Funding

TUA Research Funding
6 · The paper itself

Abstract

Porphyromonas gingivalis (P. gingivalis) is a gram-negative bacterium and an important etiologic agent of periodontitis. P. gingivalis releases outer membrane vesicles containing lipopolysaccharides (LPS), which can penetrate periodontal tissues. Once in the periodontal tissues and in contact with immune cells, it may participate in the destructive innate host response associated with the disease. The exact mechanism of P. gingivalis LPS in the disease process is not clear, but it is known to affect a variety of immune responses.

objectivesTo investigate how LPS from P. gingivalis affect neutrophil extracellular trap (NET) formation, cell death and production of cytokines from human neutrophils and peripheral mononuclear blood mononuclear cells (PBMCs). MATERIALS AND

methodsIsolated neutrophils and PBMCs were cultured with LPS from P. gingivalis or Escherichia coli (E. coli) (control). The NET formation was measured using Sytox green stain. Cell death of neutrophils and PBMCs was analyzed using flow cytometry or Sytox green stain. Cytokine production was measured using enzyme-linked immunosorbent assay (ELISA) kit or Bio-Plex assay.

resultsExposure to LPS from P. gingivalis and E. coli caused significantly lower cell death in neutrophils. NETs were formed after exposure to the two different LPS. In PBMCs, exposure to P. gingivalis and E. coli LPS caused increased levels of IL-1β and IL-6 compared to unstimulated controls. Increased cell death in PBMCs after exposure to LPS from E. coli in comparison to LPS from P. gingivalis and unstimulated controls was also observed.

conclusionsLPS from P. gingivalis has the ability to affect both human neutrophils and PBMCs with regard to cytokine production, cell death and production of NETs. LPS from P. gingivalis could be involved in the pathogenesis of periodontitis, and our results may contribute information regarding possible markers for diagnosis and targets for treatment of periodontal disease.

Indexed as

Porphyromonas gingivalisCytokinesEscherichia coliHumansLipopolysaccharidesPeriodontitisCytokinesLipopolysaccharidesEscherichia colilipopolysaccharidemononuclear leukocytesneutrophilsPorphyromonas gingivalis

Identifiers

PMID33377284
PMCPMC8404501
OpenAlexW3115962954

What OpenQuestion holds

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LicenceCC BY
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.