Evidence map›Paper›PMID 31662504›Full record

ArticleIn vivo (Athens, Greece)

EBV LMP1 in Gingival Epithelium Potentially Contributes to Human Chronic Periodontitis

Norihisa Watanabe, Keiko Nodomi, Ryo Koike, Ayako Kato, Osamu Takeichi, A I Kotani, Tadayoshi Kaneko, Hiroshi Sakagami, Masami Takei, Yorimasa Ogata and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.9field-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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. How Does Epstein-Barr Virus Contribute to Chronic Periodontitis?International journal of molecular sciences · 2020
    Review
  8. 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

12 authors at 3 institutions in 1 country.

Norihisa WatanabeDepartment of Periodontology, Nihon University School of Dentistry, Tokyo, Japan.
Keiko NodomiDepartment of Microbiology, Nihon University School of Dentistry, Tokyo, Japan.
Ryo KoikeDepartment of Microbiology, Nihon University School of Dentistry, Tokyo, Japan.
Ayako KatoDepartment of Periodontology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
Osamu TakeichiDepartment of Endodontics, Nihon University School of Dentistry, Tokyo, Japan.
A I KotaniDepartment of Hematological Malignancy, Institute of Medical Science, Tokai University, Kanagawa, Japan.
Tadayoshi KanekoDepartment of Oral and Maxillofacial Surgery, Nihon University School of Dentistry, Tokyo, Japan.
Hiroshi SakagamiMeikai University Research Institute of Odontology (M-RIO), Saitama, Japan.
Masami TakeiDivision of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Yorimasa OgataDepartment of Periodontology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
Shuichi SatoDepartment of Periodontology, Nihon University School of Dentistry, Tokyo, Japan.
Kenichi ImaiDepartment of Microbiology, Nihon University School of Dentistry, Tokyo, Japan imai.kenichi@nihon-u.ac.jp.
Nihon University · JPMeikai University · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimHuman chronic periodontitis is a major health problem. Although some oral bacteria have been reported to be putative pathogens, Epstein-Barr virus (EBV) is reported to be associated with the progression of periodontitis. However, the role of EBV in the aetiology of periodontitis is unknown. Therefore, we investigated periodontal pathogenesis of EBV to confirm whether EBV-encoded latent membrane protein 1 (LMP1) induces Interleukin-8 (IL8) production in human gingival cells. MATERIALS AND

methodsReal-time polymerase chain reaction, luciferase assay, enzyme-linked immunosorbent assay (ELISA), and western blotting were performed for determining IL8 mRNA expression, nuclear factor kappa B (NF-ĸB) transcription, IL8 production, and the phosphorylation of NF-ĸB p65 and Inhibitor of kappa B alpha (IĸBα), respectively, in Ca9-22 human gingival epithelial cells. Two LMP1 mutants lacking C-terminal activating region (CATR) domains responsible for activating NF-ĸB were used.

resultsExtremely high IL8 production was induced by LMP1 in time- and dose-dependent manner, where simultaneous phosphorylation of NF-κB p65 and IĸBα and transcription of NF-ĸB were observed. On the contrary, IL8 production and NF-ĸB transcription were drastically inhibited by dominant negative mutant of IĸBα. Moreover, the LMP1 mutants failed to induce IL8 production.

conclusionOur findings suggest that due to CATR domains, LMP1 contributes to the progression of periodontitis via IL8 production attributable to NF-ĸB activation.

Indexed as

Cell LineChronic PeriodontitisEpithelial CellsEpitheliumGingivaHerpesvirus 4, HumanHumansInterleukin-8NF-kappa BSignal TransductionTranscription Factor RelAViral Matrix ProteinsCXCL8 protein, humanEBV-associated membrane antigen, Epstein-Barr virusInterleukin-8NF-kappa BTranscription Factor RelAViral Matrix ProteinsEBVgingival epithelial cellsIL8LMP1NF-ĸBperiodontitis

Identifiers

PMID31662504
PMCPMC6899117
OpenAlexW2988667521

What OpenQuestion holds

Textmetadata
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.