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Gene Expression Profiling in Fibromyalgia Indicates an Autoimmune Origin 2020

pattismith

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Gene Expression Profiling in Fibromyalgia Indicates an Autoimmune Origin of the Disease and Opens New Avenues for Targeted Therapy

1 Department of Medicine, University of Verona, Piazzale L.A. Scuro 10, 37134 Verona, Italy
2 Department of Experimental Medicine, Section of Histology, University of Genova, Via G.B. Marsano 10, 16132 Genova, Italy

Published: 10 June 2020

Abstract
Fibromyalgia is a chronic disorder characterized by widespread pain and by several non-pain symptoms.

Autoimmunity, small fiber neuropathy and neuroinflammation have been suggested to be involved in the pathogenesis of the disease.

We have investigated the gene expression profile in peripheral blood mononuclear cells obtained from ten patients and ten healthy subjects.

Of the 545,500 transcripts analyzed, 1673 resulted modulated in fibromyalgic patients. The majority of these genes are involved in biological processes and pathways linked to the clinical manifestations of the disease.

Moreover, genes involved in immunological pathways connected to interleukin-17 and to Type I interferon signatures were also modulated, suggesting that autoimmunity plays a role in the disease.

We then aimed at identifying differentially expressed Long non-coding RNAs (LncRNAs) functionally connected to modulated genes both directly and via microRNA targeting.

Only two LncRNAs of the 298 found modulated in patients, were able to target the most highly connected genes in the fibromyalgia interactome, suggesting their involvement in crucial gene regulation.

Our gene expression data were confirmed by real time PCR, by autoantibody testing, detection of soluble mediators and Th-17 polarization in a validation cohort of 50 patients.

Our results indicate that genetic and epigenetic mechanisms as well as autoimmunity play a pivotal role in the pathogenesis of fibromyalgia.

(free full article available)
 

pattismith

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"3.6. Autoantibodies Detection in FM Patients’ Sera

Of the 60 patients (training and validation group) who were evaluated for both the early and classic SS markers, 18 (30%) tested positive for SS autoantibodies and 15 (25%) tested positive for the early tissue specific autoantibodies only.

Moreover, we assessed the antiserotonin, antiganglioside and antiphospholipid antibodies concentration in FM patients’ sera and, we found increased levels (p < 0.0001) of these antibodies in 21%, 18% and 15% of patients after comparison to healthy subjects."




So then @pattismith could fibro be helped using CRISPR?
I'm not qualified to answer, maybe someone will?
 

Pyrrhus

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Moreover, genes involved in immunological pathways connected to interleukin-17 and to Type I interferon signatures were also modulated, suggesting that autoimmunity plays a role in the disease.
None of this suggests autoimmunity...

"3.6. Autoantibodies Detection in FM Patients’ Sera
...But these DO suggest autoimmunity!