Evidence map›Paper›PMID 31693828›Full record

ArticleJournal of microbiology and biotechnology2020

Resolvin D5, a Lipid Mediator, Inhibits Production of Interleukin-6 and CCL5 Via the ERK-NF-κB Signaling Pathway in Lipopolysaccharide-Stimulated THP-1 Cells.

Hyun-Woo Chun, Jintak Lee, Thu-Huyen Pham, Jiyon Lee, Jae-Hwan Yoon, Jin Lee, Deok-Kun Oh, Jaewook Oh, Do-Young Yoon

Open access · greenAbstract read
In one paragraph

Article in Journal of microbiology and biotechnology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 39 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Hyun-Woo ChunDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Jintak LeeDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Thu-Huyen PhamDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Jiyon LeeDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Jae-Hwan YoonDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Jin LeeDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Deok-Kun OhDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Jaewook OhDepartment of Stem Cell and Regenerative Biotechnology, Konkuk University, Seoul 05029, Republic of Korea.
Do-Young YoonDepartment of Bioscience and Biotechnology, Research Institute of Bioactive-Metabolome Network, Konkuk University, Seoul 05029, Republic of Korea.
Konkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the omega-3 essential fatty acids, docosahexaenoic acid (DHA), is a significant constituent of the cell membrane and the precursor of several potent lipid mediators. These mediators are considered to be important in preventing or treating several diseases. Resolvin D5, an oxidized lipid mediator derived from DHA, has been known to exert anti-inflammatory effects. However, the detailed mechanism underlying these effects has not yet been elucidated in human monocytic THP-1 cells. In the present study, we investigated the effects of resolvin D5 on inflammation-related signaling pathways, including the extracellular signal-regulated kinase (ERK)-nuclear factor (NF)-κB signaling pathway. Resolvin D5 downregulated the production of interleukin (IL)-6 and chemokine (C-C motif) ligand 5 (CCL5). Additionally, these inhibitory effects were found to be modulated by mitogen-activated protein kinase (MAPK) and NF-κB in lipopolysaccharide (LPS)-treated THP-1 cells. Resolvin D5 inhibited the LPS-stimulated phosphorylation of ERK and translocation of p65 and p50 into the nucleus, resulting in the inhibition of IL-6 and CCL5 production. These results revealed that resolvin D5 exerts anti-inflammatory effects in LPS-treated THP-1 cells by regulating the phosphorylation of ERK and nuclear translocation of NF-kappaB.

Indexed as

Anti-Inflammatory AgentsCell SurvivalChemokine CCL5Docosahexaenoic AcidsDown-RegulationHumansInflammationInterleukin-6LipopolysaccharidesMAP Kinase Signaling SystemMonocytesPhosphorylationSignal TransductionTHP-1 CellsAnti-Inflammatory AgentsCCL5 protein, humanChemokine CCL5Docosahexaenoic AcidsIL6 protein, humanInterleukin-6Lipopolysaccharidesresolvin D5anti-inflammatoryERKNF-κBResolvin D5THP-1 cells

Identifiers

PMID31693828
PMCPMC9728331
OpenAlexW2990737972

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.