Evidence map›Paper›PMID 38228433›Full record

ArticleInternational dental journal2024

Epstein-Barr Virus Promotes Inflammatory Cytokine Production in Human Gingival Fibroblasts.

Wenmin Zeng, Guojing Liu, Qingxian Luan, Chunyu Yang, Xin Luo, Zijun Zhu, Xiaoqian Yu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International dental journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

7 authors.

Wenmin ZengDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases, Beijing, China.
Guojing LiuDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases, Beijing, China.
Qingxian LuanDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases, Beijing, China.
Chunyu YangDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases, Beijing, China.
Xin LuoDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases, Beijing, China.
Zijun ZhuDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases, Beijing, China.
Xiaoqian YuDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases, Beijing, China. Electronic address: y_pk@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPeriodontitis is one of the most common chronic oral inflammatory diseases. Over the past decade, herpes viruses, particularly Epstein-Barr virus (EBV), have been considered promising pathogenic candidates for periodontitis. However, the specific mechanism by which EBV contributes to the development of periodontitis is still unknown. This study aimed to explore the mechanism of EBV underlying the inflammatory response in human gingival fibroblasts (HGFs). MATERIALS AND

methodsHGFs were stimulated with different concentrations of EBV (10

resultsThe expressions of IL-1β, TNF-α, IL-8, and MCP-1 were significantly upregulated in HGFs under EBV stimulation in a concentration- and time-dependent manner. EBV promoted TLR9 and MyD88 expression and induced NF-κB transcription. On the contrary, the upregulation of these factors and the activation of NF-κB pathway were drastically inhibited by TLR9 antagonists.

conclusionsOur findings demonstrate that EBV promotes the production of inflammatory cytokines IL-1β and TNF-α and chemokines IL-8 and MCP-1 in HGFs through the TLR9/MyD88/NF-κB pathway.

Indexed as

Chemokine CCL2CytokinesFibroblastsGingivaHerpesvirus 4, HumanInterleukin-1betaToll-Like Receptor 9Cells, CulturedEnzyme-Linked Immunosorbent AssayHumansInterleukin-8Myeloid Differentiation Factor 88NF-kappa BPeriodontitisReal-Time Polymerase Chain ReactionRNA, MessengerCCL2 protein, humanChemokine CCL2CytokinesInterleukin-1betaInterleukin-8Myeloid Differentiation Factor 88NF-kappa BRNA, MessengerTLR9 protein, humanToll-Like Receptor 9Tumor Necrosis Factor-alphaEpstein-Barr virusHuman gingival fibroblastsPeriodontitisProinflammatory cytokines

Identifiers

PMID38228433
PMCPMC11123576

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.