Evidence map›Paper›PMID 36088483›Full record

ArticleScientific reports2022

Toll-like receptor 4-mediated endoplasmic reticulum stress induces intestinal paneth cell damage in mice following CLP-induced sepsis.

Yijie Wang, Dapeng Zhang, Congxin Li, Xue Wu, Chen He, Xiaolin Zhu, Haiyan Zhao, Lingjie Mu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. LRRK2NPJ Parkinson's disease · 2026
    Article
  4. Article
  5. Article
  6. Intestinal injury signaling pathway in sepsis.Frontiers in immunology · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. 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

8 authors at 2 institutions in 1 country.

Yijie Wang *Department of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, Kunming, China. 81543505@qq.com.
Dapeng Zhang *Department of Internal Medicine, Kunming Meizhao Physical Examination Center, Kunming, China.
Congxin LiDepartment of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Xue WuDepartment of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Chen HeDepartment of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Xiaolin ZhuDepartment of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Haiyan ZhaoDepartment of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Lingjie MuDepartment of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
First Affiliated Hospital of Kunming Medical University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A marked elevation of TLR4 was observed in various organs of septic mice. The mechanism of TLR4 in intestinal epithelial cell damage in sepsis remains unclear. CLP mice models were used to assess the role of TLR4 in intestinal Paneth cell damage by histological, polymerase chain reaction, western-blot analyses. The ileal expression of TLR4 was increased by more than five-fold after CLP. CLP significantly increased 7-day mortality and was associated with a higher murine sepsis score (MSS), closely related with increased TLR4 expression. Histological staining revealed that a reduced number of Paneth cells, accompanied by reduced lysozyme and defensin alpha 5(DEF-5) expression as detected by PCR. Of note, the expression levels of ATF6, XBP1 and CHOP increased in the ileal of the sepsis group. Meanwhile, the uncleaved p90 ATF6 was markedly reduced and cleaved p50 ATF6 was increased in the sepsis group. Intriguingly, The TAK-242 had improved intestinal mucosal injury, reduced the expression of ATF6, XBP1 and CHOP and relieved the cleavage of ATF6. We found that increased the expression level of TLR4 in the ileal of CLP mice promoted the depletion of Paneth cell and reduced LYZ and DEF-5 expression. Furthermore, our findings suggested that TLR4-mediated the hyperactivation of ER stress, via activating the ATF6/CHOP pathway, might be one of the mechanisms associated with Paneth cells loss and dysfunction during intestinal barrier impairment of sepsis.

Indexed as

Paneth CellsSepsisAnimalsEndoplasmic Reticulum StressIntestinesMiceToll-Like Receptor 4Toll-Like Receptor 4

Identifiers

PMID36088483
PMCPMC9464222
OpenAlexW4295423227

What OpenQuestion holds

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LicenceCC BY
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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.