Evidence map›Paper›PMID 28537905›Full record

ArticleOncotarget2017

Suppression of LPS-induced inflammatory responses by the hydroxyl groups of dexamethasone.

Ting-Yun Chuang, An-Jie Cheng, I-Ting Chen, Tien-Yun Lan, I-Hsuan Huang, Chung-Wai Shiau, Chia-Lin Hsu, Ya-Wen Liu, Zee-Fen Chang, Ping-Hui Tseng and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

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  13. The Anti-Inflammatory Effects of Broccoli (Current issues in molecular biology · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Comparison of the in vitro Anti-Inflammatory Effect of Cannabidiol to Dexamethasone.Clinical, cosmetic and investigational dermatology · 2022
    Article
  18. Article
  19. Review
  20. 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

11 authors at 3 institutions in 1 country.

Ting-Yun ChuangInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
An-Jie ChengInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
I-Ting ChenInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
Tien-Yun LanInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
I-Hsuan HuangInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
Chung-Wai ShiauInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei 11221, Taiwan.
Chia-Lin HsuInstitute of Microbiology and Immunology, National Yang-Ming University, Taipei 11221, Taiwan.
Ya-Wen LiuInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 10002, Taiwan.
Zee-Fen ChangInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 10002, Taiwan.
Ping-Hui TsengInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
Jean-Cheng KuoInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 11221, Taiwan.
National Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The innate immune response is a central process that is activated during pathogenic infection in order to maintain physiological homeostasis. It is well known that dexamethasone (Dex), a synthetic glucocorticoid, is a potent immunosuppressant that inhibits the cytokine production induced by bacterial lipopolysaccharides (LPS). Nevertheless, the extent to which the functional groups of Dex control the excessive activation of inflammatory reactions remains unknown. Furthermore, importantly, the role of Dex in the innate immune response remains unclear. Here we explore the mechanism of LPS-induced TNF-α secretion and reveal p38 MAPK signaling as a target of Dex that is involved in control of tumor necrosis factor-α (TNF-α)-converting enzyme (TACE) activity; that later mediates the shedding of TNF-α that allows its secretion. We further demonstrate that the 11-hydroxyl and 21-hydroxyl groups of Dex are the main groups that are involved in reducing LPS-induced TNF-α secretion by activated macrophages. Blockage of the hydroxyl groups of Dex inhibits immunosuppressant effect of Dex during LPS-induced TNF-α secretion and mouse mortality. Our findings demonstrate Dex signaling is involved in the control of innate immunity.

Indexed as

AcetylationADAM17 ProteinAnimalsAnti-Inflammatory AgentsDexamethasoneHydroxidesInflammationLipopolysaccharidesMacrophage ActivationMacrophagesMAP Kinase Signaling SystemMiceModels, BiologicalMolecular StructureRAW 264.7 CellsTumor Necrosis Factor-alphaADAM17 ProteinAnti-Inflammatory AgentsDexamethasonehydroxide ionHydroxidesLipopolysaccharidesTumor Necrosis Factor-alphadexamethasoneinnate immunityp38 MAPK signalingTNF-α secretiontumor necrosis factor-α (TNF-α)-converting enzyme

Identifiers

PMID28537905
PMCPMC5564803
OpenAlexW2613012234

What OpenQuestion holds

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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.