Evidence map›Paper›PMID 35054995›Full record

ArticleInternational journal of molecular sciences2022

Epstein-Barr Virus Promotes the Production of Inflammatory Cytokines in Gingival Fibroblasts and RANKL-Induced Osteoclast Differentiation in RAW264.7 Cells.

Sho Yokoe, Akira Hasuike, Norihisa Watanabe, Hideki Tanaka, Hiroyuki Karahashi, Shin Wakuda, Osamu Takeichi, Takayuki Kawato, Hideki Takai, Yorimasa Ogata and 2 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

12 authors.

Sho YokoeDepartment of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Akira HasuikeDepartment of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.ORCID 0000-0001-5150-2076
Norihisa WatanabeDepartment of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Hideki TanakaDepartment of Oral Health Sciences, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Hiroyuki KarahashiDepartment of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Shin WakudaDepartment of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Osamu TakeichiDepartment of Endodontics, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Takayuki KawatoDepartment of Oral Health Sciences, Nihon University School of Dentistry, Tokyo 101-8310, Japan.ORCID 0000-0001-9831-9455
Hideki TakaiDepartment of Periodontology, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Japan.
Yorimasa OgataDepartment of Periodontology, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Japan.ORCID 0000-0002-2767-844X
Shuichi SatoDepartment of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.
Kenichi ImaiDepartment of Microbiology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.ORCID 0000-0003-0985-4267

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis is an inflammatory condition that causes the destruction of the supporting tissues of teeth and is a major public health problem affecting more than half of the adult population worldwide. Recently, members of the herpes virus family, such as the Epstein-Barr virus (EBV), have been suggested to be involved in the etiology of periodontitis because bacterial activity alone does not adequately explain the clinical characteristics of periodontitis. However, the role of EBV in the etiology of periodontitis is unknown. This study aimed to examine the effect of inactivated EBV on the expression of inflammatory cytokines in human gingival fibroblasts (HGFs) and the induction of osteoclast differentiation. We found that extremely high levels of interleukin (IL)-6 and IL-8 were induced by inactivated EBV in a copy-dependent manner in HGFs. The levels of IL-6 and IL-8 in HGFs were higher when the cells were treated with EBV than when treated with lipopolysaccharide and lipoteichoic acid. EBV induced IκBα degradation, NF-κB transcription, and RAW264.7 cell differentiation into osteoclast-like cells. These findings suggest that even without infecting the cells, EBV contributes to inflammatory cytokine production and osteoclast differentiation by contact with oral cells or macrophage lineage, resulting in periodontitis onset and progression.

Indexed as

Host-Pathogen InteractionsAnimalsCell DifferentiationCells, CulturedCytokinesEpstein-Barr Virus InfectionsGene ExpressionGingivaHerpesvirus 4, HumanInflammation MediatorsMiceOsteoclastsRANK LigandRAW 264.7 CellsSignal TransductionCytokinesInflammation MediatorsRANK LigandEpstein–Barr virusgingival fibroblastsosteoclastperiodontitisproinflammatory cytokines

Identifiers

PMID35054995
PMCPMC8775710

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.