Fibromyalgia and microglial TNF-α: Translational research using human blood induced microglia-like cells
Open accessAbstract
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.
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In human iMG cells from FMS patients exposed to ATP in vitro, there is a moderate correlation between NPP and ATP-induced upregulation of TNF-α expression.
“Masahiro Ohgidani et al. generated human-induced microglia-like (iMG) cells from FMS patients with FMS and exposed them to ATP in vitro, identifying a moderate correlation between NPP and ATP-induced upregulation of TNF-α expression (136).”
From Nociplastic pain: the prominent role of non-neuronal cells in central and peripheral sensitization (2026) · cites this paper as [136]
The paper’s correlation analysis (Introduction, Fig. 2; page not specified) reports moderate positive correlations between ATP-stimulated iMG-cell TNF-α expression and subjective pain intensity and interference. It does not identify or report an NPP measure, so that specific part of the claim is not supported by our copy. (LLM, conf=0.84)
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“Masahiro Ohgidani et al. generated human-induced microglia-like (iMG) cells from FMS patients with FMS and exposed them to ATP in vitro , identifying a moderate correlation between NPP and ATP-induced upregulation of TNF-a expression (136).”
- Authors
- Ohgidani, M., Kato, T. A., Hosoi, M., Tsuda, M., Hayakawa, K., Hayaki, C., Iwaki, R., Sagata, N., Hashimoto, R., Inoue, K., Sudo, N., & Kanba, S.
- Affiliations
- Kyushu University (JP)
- Kyushu University Hospital (JP)
- The University of Osaka (JP)
- Corresponding author
- Kato, Takahiro A.
- ORCID
- Venue
- Scientific Reports
- Published
- 2017-09-19
- Volume
- 7
- Issue
- 1
- Pages
- 11882-11882
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5605512
- OpenAlex
- W2754547625
- Cited by
- 49
- References
- 3
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 6 · 2023: 8 · 2022: 5 · 2021: 2 · 2020: 6 · 2019: 5 · 2018: 4
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Kyushu University Institutional Repository (QIR) (Kyushu University) (submittedVersion, cc-by)
- Funders
- Japan Agency for Medical Research and Development
- SENSHIN Medical Research Foundation
- Japan Society for the Promotion of Science (25117011, 26713039, 25117013, 17K09304, 17K19915)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Keywords
- fibromyalgia, microglia, TNF-α, peripheral blood monocytes, ATP stimulation, chronic pain, microglial activation, subjective pain, neuroinflammation
- MeSH terms
- Adenosine Triphosphate, Female, Fibromyalgia, Gene Expression Regulation, Humans, Male, Monocytes, Tumor Necrosis Factor-alpha, Microglia, Translational Research, Biomedical
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