Evidence map›Paper›PMID 37017858›Full record

ArticleInflammation2023

E. coli LPS/TLR4/NF-κB Signaling Pathway Regulates Th17/Treg Balance Mediating Inflammatory Responses in Oral Lichen Planus.

Mengna Zhang, Linglin Wang, Chenyu Zhou, Jia Wang, Juehua Cheng, Yuan Fan

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Article
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  9. Article
  10. Review
  11. Frontiers in cellular and infection microbiology · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Association betweenHeliyon · 2024
    Article
  17. 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

6 authors at 2 institutions in 1 country.

Mengna Zhang *Department of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
Linglin Wang *Department of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
Chenyu ZhouDepartment of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
Jia WangDepartment of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
Juehua ChengDepartment of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
Yuan FanDepartment of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China. fanyuan@njmu.edu.cn.
Nanjing Medical University · CNShanghai Stomatological Hospital · CN

Funding

Jiangsu Provincial Key Research and Development Program Grant Nos. BE2021723National Natural Science Foundation of China 81970941Priority Academic Program Development of Jiangsu Higher Education Institutions PAPD, 2018-87
6 · The paper itself

Abstract

Oral lichen planus (OLP) is a chronic inflammatory autoimmune disease mediated by T cells. The imbalance of microflora has potential impacts on the onset and development of OLP, but the mechanism is still unclear. Here, we investigated the effects of Escherichia coli (E. coli) lipopolysaccharide (LPS) simulating the microbial enrichment state of OLP on T cell immune functions in vitro. Effect of E. coli LPS on the viability of T cell using CCK8 assay. After E. coli LPS pretreatment, the expression of the toll-like receptor 4 (TLR4), nuclear factor-kappa B p65 (NF-κB p65), cytokines, retinoic acid-related orphan receptor γt (RORγt), and forkhead box p3 (Foxp3) in the peripheral blood of OLP patients and normal controls (NC) were assessed using quantitative RT-PCR (qRT-PCR), western blot, and enzyme-linked immunosorbent assay (ELISA). Finally, Th17 and Treg cells were detected by flow cytometry. We found that the TLR4/NF-κB pathway was activated and the expression of interleukin (IL)-6 and IL-17 was increased in both groups after E. coli LPS stimulation. CC chemokine ligand (CCL)20 and CC chemokine receptor (CCR)4 expression was increased in OLP after E. coli LPS treatment, while no difference was found in CCR6 and CCL17 expression of both groups. Moreover, E. coli LPS treatment enhanced the proportion of Th17 cells, Th17/Treg ratio, and RORγt/Foxp3 ratio in OLP. In conclusion, E. coli LPS regulated Th17/Treg balance to mediate the inflammatory responses of OLP through the TLR4/NF-κB pathway in vitro, indicating that oral microbiota dysbiosis affected the chronic inflammatory state of OLP.

Indexed as

Lichen Planus, OralNF-kappa BEscherichia coliForkhead Transcription FactorsHumansInterleukin-6LipopolysaccharidesNuclear Receptor Subfamily 1, Group F, Member 3Signal TransductionTh17 CellsT-Lymphocytes, RegulatoryToll-Like Receptor 4Forkhead Transcription FactorsInterleukin-6LipopolysaccharidesNF-kappa BNuclear Receptor Subfamily 1, Group F, Member 3TLR4 protein, humanToll-Like Receptor 4E. coli LPSinflammatoryOLPT cellTh17/Treg

Identifiers

PMID37017858
OpenAlexW4362601648

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.