HMN 2025: How Mice develop fibromyalgia-like ache after receiving intestine microbiota from human sufferers

Fibromyalgia symptoms transferred to mice through microbiota transplant
Schematic illustration of the research design. Credit: Neuron (2025). DOI: 10.1016/j.neuron.2025.03.032

McGill University-led analysis has found that transplanting intestine microbiota from girls with fibromyalgia into mice induces ache, immune activation, metabolomic adjustments, and decreased pores and skin innervation.

The actual explanation for is unknown. Fibromyalgia impacts 2% to 4% of the inhabitants, primarily girls, and is characterised by , fatigue, sleep disruptions, and cognitive difficulties. Most sufferers endure from vital signs that negatively affect high quality of life.

Dysregulated exercise of the central nervous system, altered neurotransmitters, neuroinflammation, and decreased intraepidermal nerve fiber density have been noticed in fibromyalgia sufferers. Functional gastrointestinal problems and despair are additionally frequent.

Previous research have revealed that differs between girls with fibromyalgia and wholesome controls, but the connection between this altered microbiota and any useful position it’d play stays a thriller.

In the research, “The intestine microbiota promotes ache in fibromyalgia,” published in Neuron, researchers performed a fecal microbiota transplantation study to find out whether or not altered intestine microbiota from fibromyalgia sufferers may trigger ache and associated signs.

Researchers carried out fecal microbiota transplantation (FMT) into germ-free feminine mice utilizing samples collected from girls with fibromyalgia and age-matched wholesome controls. An open-label scientific trial enrolled 14 girls with extreme fibromyalgia who obtained 5 oral FMT doses from wholesome feminine donors.

To assess ache and systemic adjustments in mice, the research employed behavioral assays, single-cell RNA sequencing, metabolomic profiling, dorsal root ganglia calcium imaging, and spinal microglia evaluation. Clinical individuals obtained oral FMT capsules biweekly for 5 doses following antibiotic and bowel cleaning preparation.

Mice that obtained microbiota from fibromyalgia sufferers developed mechanical, warmth, and chilly hypersensitivity, spontaneous ache, and muscle ache inside 4 weeks. Persistent ache and depression-like behaviors had been noticed in mice 4 months post-transplantation.

Changes coincided with altered intestine microbiota composition, marked by classical monocytes and spinal microglia, shifts in amino acid and bile acid metabolism, and decreased intraepidermal nerve fiber density. Replacing fibromyalgia-associated microbiota with that from wholesome donors reversed ache hypersensitivity. Oral bile acid supplementation additionally decreased ache responses in mice.

In the human scientific study, 14 girls with extreme, treatment-resistant fibromyalgia obtained FMT from wholesome donors. Post-treatment, 12 individuals reported a clinically vital discount in ache.

Improvements, whereas not full reversals, had been noticed in total symptom burden, sleep high quality, nervousness, and despair scores. Quantitative sensory testing confirmed reductions in chilly ache hypersensitivity. Stool evaluation confirmed profitable bacterial engraftment from wholesome donors.

Based on the outcomes, alterations in intestine microbiota could play a causal position within the growth of ache and different signs related to fibromyalgia. Because the human trial was open-label, lacked a {control} arm, and enrolled solely girls, the findings are preliminary and want affirmation in randomized managed trials.

Modulating the intestine microbiota by way of fecal transplantation presents a possible therapeutic technique for people affected by this continual ache syndrome. Establishing the useful significance of intestine microbiota in fibromyalgia would open new alternatives for evaluating microbial-based interventions.

More data:
Weihua Cai et al, The intestine microbiota promotes ache in fibromyalgia, Neuron (2025). DOI: 10.1016/j.neuron.2025.03.032

© 2025

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