Evidence map›Paper›PMID 28928366›Full record

ArticleScientific reports2017

Fibromyalgia and microglial TNF-α: Translational research using human blood induced microglia-like cells.

Masahiro Ohgidani, Takahiro A Kato, Masako Hosoi, Makoto Tsuda, Kohei Hayakawa, Chie Hayaki, Rie Iwaki, Noriaki Sagata, Ryota Hashimoto, Kazuhide Inoue and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  12. Psoriasis and Fibromyalgia: A Systematic Review.Journal of personalized medicine · 2024
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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

12 authors at 3 institutions in 1 country.

Masahiro OhgidaniDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Takahiro A KatoDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan. takahiro@npsych.med.kyushu-u.ac.jp.
Masako HosoiDepartment of Psychosomatic Medicine, Kyushu University Hospital, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Makoto TsudaDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Kohei HayakawaDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Chie HayakiDepartment of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Rie IwakiDepartment of Psychosomatic Medicine, Kyushu University Hospital, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Noriaki SagataDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Ryota HashimotoResearch Center for Children's Mental Development, United Graduate School of Child Development, Osaka University, Yamadaoka 1-1, Suita, Osaka, 565-0871, Japan.ORCID 0000-0002-5941-4238
Kazuhide InoueDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Nobuyuki SudoDepartment of Psychosomatic Medicine, Kyushu University Hospital, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Shigenobu KanbaDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Kyushu University · JPKyushu University Hospital · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibromyalgia is a refractory disease characterized by chronic intractable pain and psychological suffering, the cause of which has not yet been elucidated due to its complex pathology. Activation of immune cells in the brain called microglia has attracted attention as a potential underlying pathological mechanism in chronic pain. Until recently, however, technological and ethical considerations have limited the ability to conduct research using human microglia. To overcome this limitation, we have recently developed a technique to create human-induced microglia-like (iMG) cells from human peripheral blood monocytes. In this study, we created the iMG cells from 14 patients with fibromyalgia and 10 healthy individuals, and compared the activation of iMG cells between two groups at the cellular level. The expression of tumor necrosis factor (TNF)-α at mRNA and protein levels significantly increased in ATP-stimulated iMG cells from patients with fibromyalgia compared to cells from healthy individuals. Interestingly, there was a moderate correlation between ATP-induced upregulation of TNF-α expression and clinical parameters of subjective pain and other mental manifestations of fibromyalgia. These findings suggest that microglia in patients with fibromyalgia are hypersensitive to ATP. TNF-α from microglia may be a key factor underlying the complex pathology of fibromyalgia.

Indexed as

Gene Expression RegulationAdenosine TriphosphateFemaleFibromyalgiaHumansMaleMicrogliaMonocytesTranslational Research, BiomedicalTumor Necrosis Factor-alphaAdenosine TriphosphateTumor Necrosis Factor-alpha

Identifiers

PMID28928366
PMCPMC5605512
OpenAlexW2754547625

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.