Evidence map›Paper›PMID 33174138›Full record

ArticleInflammation2021

Silencing TLR4/MyD88/NF-κB Signaling Pathway Alleviated Inflammation of Corneal Epithelial Cells Infected by ISE.

Liucheng Wu, Lili Du, Qianqian Ju, Zhiheng Chen, Yu Ma, Ting Bai, Guiqing Ji, Yu Wu, Zhaoguo Liu, Yixiang Shao and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Sulfur Vacancy-Rich MoSAdvanced healthcare materials · 2026
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  12. β-Sitosterol Alleviates Neuropathic Pain by Affect Microglia Polarization through Inhibiting TLR4/NF-κB Signaling Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Article
  13. Article
  14. Whole Transcriptome Analysis of Intervention Effect ofCurrent issues in molecular biology · 2023
    Article
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  16. Review
  17. Review
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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

11 authors at 2 institutions in 1 country.

Liucheng Wu *Laboratory Animal Center, Nantong University, Nantong, 226001, China.
Lili Du *Laboratory Animal Center, Nantong University, Nantong, 226001, China.
Qianqian JuDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Zhiheng ChenLaboratory Animal Center, Nantong University, Nantong, 226001, China.
Yu MaLaboratory Animal Center, Nantong University, Nantong, 226001, China.
Ting BaiSchool of Nursing, Nantong University, Nantong, 226001, China.
Guiqing JiLaboratory Animal Center, Nantong University, Nantong, 226001, China.
Yu WuPharmacy Department, Nantong Hospital of Traditional Chinese Medicine, Nantong, 226001, China.
Zhaoguo LiuSchool of Pharmacy, Nantong University, Nantong, 226001, China.
Yixiang ShaoLaboratory Animal Center, Nantong University, Nantong, 226001, China.
Xiaoqing PengLaboratory Animal Center, Nantong University, Nantong, 226001, China. pxq@ntu.edu.cn.ORCID http://orcid.org/0000-0003-0156-9138
Nantong University · CNAnyang Hospital of Traditional Chinese Medicine · CN

Funding

Nantong Science and Technology Bureau (CN) JC2018090Natural Science Foundation of Jiangsu Province 15KJB180015Scientific Innovation Research of College Graduates in Jiangsu Province KYCX18-2415
6 · The paper itself

Abstract

The regulatory role of toll-like receptor 4 (TLR4) in the inactivate staphylococcus epidermidis (ISE)-induced cornea inflammation is not well investigated. Here, TLR4 silence could decrease inflammatory cytokines in corneal epithelial cells treated with ISE. The mouse corneal epithelial cells were exposed to ISE for 24 h, either alone or with the NF-κB inhibitor, TLR4 lentivirus to bilaterally (knock-down or and overexpression). The expression of TLR4 in mouse corneal epithelial cells was investigated using western blot and qRT-PCR assay. The inflammatory cytokine levels were evaluated by qRT-PCR and ELISA, respectively. The relative impact factors of TLR4-mediated NF-κB signaling detected using western blot assay. Results show the expression levels of TLR4 and some inflammatory cytokines were significantly increased in corneal epithelial cells treated with ISE. TLR4 Silence markedly decreased ISE-induced production of IL12, TNF-α, CCL5, and CCL9 in corneal epithelial cells. Furthermore, the nuclear translocation of NF-κB p65 and myeloid differentiation protein 88 (MyD88) in the cells treated with ISE were further reduced by silencing TLR4. Inhibition of TLR4-mediated NF-κB signaling by using BAY11-7082 also alleviated ISE-induced inflammation. In the rescue experiment, transfected the stable TLR4 silenced corneal epithelial cells with TLR4 overexpression lentivirus, we found that TLR4 overexpression can restore the down-regulation of TLR4 and inflammatory cytokines (IL12, TNF-α, CCL9) caused by TLR4 knocked down. Therefore, ISE-induced cornea inflammation was due to the activation of the TLR4/MyD88/NF-κB signaling pathway, and dramatically stimulated IL12, TNF-α, CCL9 secretion. TLR4 silence presented mitigates damage in corneal epithelial cells treated with ISE.

Indexed as

AnimalsAnti-Inflammatory AgentsBiomarkersBlotting, WesternCytokinesEpithelial CellsEpithelium, CornealGene SilencingKeratitisMiceMice, Inbred C57BLMyeloid Differentiation Factor 88NF-kappa BNitrilesReverse Transcriptase Polymerase Chain ReactionSignal Transduction3-(4-methylphenylsulfonyl)-2-propenenitrileAnti-Inflammatory AgentsBiomarkersCytokinesMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BNitrilesSulfonesTlr4 protein, mouseToll-Like Receptor 4corneal epithelial cellsinactivate staphylococcus epidermidisinflammationinflammatory cytokinesNF-κBtoll-like receptor 4

Identifiers

PMID33174138
OpenAlexW3098581360

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.