Evidence map›Paper›PMID 38542287›Full record

ArticleInternational journal of molecular sciences2024

Vesicular Messages from Dental Biofilms for Neutrophils.

Ljubomir Vitkov, Jelena Krunić, Johanna Dudek, Madhusudhan Reddy Bobbili, Johannes Grillari, Bernhard Hausegger, Irena Mladenović, Nikola Stojanović, Wolf Dietrich Krautgartner, Hannah Oberthaler and 5 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
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  5. 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

15 authors at 5 institutions in 3 countries.

Ljubomir VitkovDepartment of Dental Pathology, Faculty of Medicine, University of East Sarajevo, 73300 Foča, Bosnia and Herzegovina.ORCID 0000-0002-1249-0161
Jelena KrunićDepartment of Dental Pathology, Faculty of Medicine, University of East Sarajevo, 73300 Foča, Bosnia and Herzegovina.ORCID 0000-0001-5081-318X
Johanna DudekClinic of Operative Dentistry, Periodontology and Preventive Dentistry, Saarland University, 664241 Homburg, Germany.
Madhusudhan Reddy BobbiliLudwig Boltzmann Institute for Traumatology, Research Center in Cooperation with AUVA, 1200 Vienna, Austria.ORCID 0000-0001-9955-0675
Johannes GrillariLudwig Boltzmann Institute for Traumatology, Research Center in Cooperation with AUVA, 1200 Vienna, Austria.ORCID 0000-0001-5474-6332
Bernhard HauseggerDepartment of Environment & Biodiversity, University of Salzburg, 5020 Salzburg, Austria.
Irena MladenovićDepartment of Oral Rehabilitation, Faculty of Medicine, University of East Sarajevo, 73300 Foča, Bosnia and Herzegovina.ORCID 0000-0002-3044-6156
Nikola StojanovićDepartment of Oral Rehabilitation, Faculty of Medicine, University of East Sarajevo, 73300 Foča, Bosnia and Herzegovina.
Wolf Dietrich KrautgartnerDepartment of Environment & Biodiversity, University of Salzburg, 5020 Salzburg, Austria.
Hannah OberthalerDepartment of Environment & Biodiversity, University of Salzburg, 5020 Salzburg, Austria.
Christine SchauerDepartment of Internal Medicine 3-Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany.
Martin HerrmannDepartment of Internal Medicine 3-Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany.ORCID 0000-0002-0258-2484
Jeeshan SinghDepartment of Internal Medicine 3-Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany.ORCID 0000-0003-0448-288X
Bernd MinnichDepartment of Environment & Biodiversity, University of Salzburg, 5020 Salzburg, Austria.ORCID 0000-0003-1218-1913
Matthias HannigClinic of Operative Dentistry, Periodontology and Preventive Dentistry, Saarland University, 664241 Homburg, Germany.
University of Salzburg · ATFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of East Sarajevo · BAInstitute of Molecular Biotechnology · ATSaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The encounter between dental biofilm and neutrophils in periodontitis remains elusive, although it apparently plays a crucial role in the periodontal pathology and constitutes a key topic of periodontology. Dental biofilm and neutrophils were isolated from orally healthy persons and patients with periodontitis. We investigated biofilm and its particle-shedding phenomenon with electron microscopy and nanoparticle tracking analysis (NTA); biofilm shedding-neutrophil interactions were examined ex vivo with epi-fluorescence microscopy. For this purpose, we used acellular dental biofilm shedding, purified lipopolysaccharide (LPS), and phorbol 12-myristate 13-acetate (PMA) as activators, and the interleukin 8 receptor beta (CXCR2) inhibitor and the anti-interleukin 8 receptor alpha (CXCR1) antibody as modulators. The shedding of acellular dental biofilms overwhelmingly consists of bacterial extracellular vesicles (BEVs). The latter induced the moderate formation of neutrophil extracellular traps (NETs) in orally healthy subjects and a strong formation in patients with periodontitis. A CXCR2 inhibitor and an anti-CXCR1 antibody had a minor effect on NET formation. Neutrophils from patients with periodontitis exhibited NET hyper-responsiveness. BEVs were stronger inducers of NET formation than purified LPS and PMA. A plateau of neutrophil responsiveness is reached above the age of 40 years, indicating the abrupt switch of maladaptive trained immunity (TI) into the activated modus. Our results suggest that dental biofilms consist of and disseminate immense amounts of outer membrane vesicles (OMVs), which initiate NET formation via a non-canonical cytosolic LPS/caspase-4/11/Gasdermin D pathway. This modus of NET formation is independent of neutrophil elastase (NE), myeloperoxidase (MPO), peptidylarginine deiminase 4 (PAD4), and toll-like receptors (TLR). In periodontitis, the hyper-responsiveness of neutrophils to BEVs and the increased NET formation appear to be a consequence of TI.

Indexed as

Extracellular TrapsPeriodontitisAdultBiofilmsHumansLipopolysaccharidesNeutrophilsLipopolysaccharidesbacterial extracellular vesiclescaspase 4dental biofilmouter membrane vesiclesperiodontitistrained immunity

Identifiers

PMID38542287
PMCPMC10970663
OpenAlexW4392847551

What OpenQuestion holds

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Registered trials

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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.