Evidence map›Paper›PMID 35684042›Full record

ArticleNutrients2022

Gene Set Enrichment Analysis Reveals That Fucoidan Induces Type I IFN Pathways in BMDC.

Suyoung Choi, Sol A Jeon, Bu Yeon Heo, Ju-Gyeong Kang, Yunju Jung, Pham Thi Thuy Duong, Ik-Chan Song, Jeong-Hwan Kim, Seon-Young Kim, Jaeyul Kwon

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-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

6 citing papers in PubMed, 12 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

10 authors at 3 institutions in 1 country.

Suyoung ChoiDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Sol A JeonPersonalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
Bu Yeon HeoDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Ju-Gyeong KangDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.
Yunju JungDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Pham Thi Thuy DuongDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Ik-Chan SongDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Jeong-Hwan KimPersonalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
Seon-Young KimPersonalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.ORCID 0000-0002-1030-7730
Jaeyul KwonDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.ORCID 0000-0002-2452-4111
Chungnam National University · KRKorea Research Institute of Bioscience and Biotechnology · KRKorea Advanced Institute of Science and Technology · KR

Funding

Chungnam National University research fundthe National Research Foundation of Korea (NRF) NRF 2019R1I1A3A01060331
6 · The paper itself

Abstract

Fucoidan, a sulfated polysaccharide extracted from brown seaweed, has been proposed to effectively treat and prevent various viral infections. However, the mechanisms behind its antiviral activity are not completely understood. We investigate here the global transcriptional changes in bone marrow-derived dendritic cells (BMDCs) using RNA-Seq technology. Through both analysis of differentially expressed genes (DEG) and gene set enrichment analysis (GSEA), we found that fucoidan-treated BMDCs were enriched in virus-specific response pathways, including that of SARS-CoV-2, as well as pathways associated with nucleic acid-sensing receptors (RLR, TLR, NLR, STING), and type I interferon (IFN) production. We show that these transcriptome changes are driven by well-known regulators of the inflammatory response against viruses, including IRF, NF-κB, and STAT family transcription factors. Furthermore, 435 of the 950 upregulated DEGs are classified as type I IFN-stimulated genes (ISGs). Flow cytometric analysis additionally showed that fucoidan increased MHCII, CD80, and CD40 surface markers in BMDCs, indicative of greater antigen presentation and co-stimulation functionality. Our current study suggests that fucoidan transcriptionally activates PRR signaling, type I IFN production and signaling, ISGs production, and DC maturation, highlighting a potential mechanism of fucoidan-induced antiviral activity.

Indexed as

COVID-19Dendritic CellsAntiviral AgentsHumansPolysaccharidesSARS-CoV-2Antiviral AgentsfucoidanPolysaccharidesantiviralBMDCdendritic cellsdifferentially expressed genes (DEGs)fucoidangene set enrichment analysis (GSEA)innate immune cellsPRRSARS-CoV-2type I IFN

Identifiers

PMID35684042
PMCPMC9182765
OpenAlexW4281628105

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.