29 april 2025: Bron: Nature Neuron d.d. 24 april 2025

Wanneer bij vrouwen met chronische fibromyalgie hun darmflora - darmmicrobioom wordt gestimuleerd door FMT = fecale microbiota transplantaties met darmbacteriën van aantoonbaar gezonde mensen dan verbetert dit de kwaliteit van leven aanzienlijk en ervaren de patiënten met fibromyalgie veel minder pijn dan daarvoor. Deze eerste studie bij mensen bevestigt ook de resultaten behaald met verschillende muizenstudies. Uit eerdere studies is ook aangetoond dat mensen met fybromyalgie een andere samenstelling hebben van hun darmflora - darmmicrobioom in vergelijking met de darmflora - darmmicrobioom van gezonde mensen.

De onderzoekers hebben in muizenstudies eerder aangetoond dat de darmflora - darmmicrobioom van patiënten met fibromyalgie indien ingebracht bij muizen pijn veroorzaakt plus depressiviteit, verwardheid soms, slapeloosheid enz. in tegenstelling tot die van gezonde mensen. 

Het studieverslag van de 14 vrouwen laat zien dat 11 van de 14 vrouwen de 5 transplantaties kregen en 12 van de veertien aanzienlijk minder pijn ervaarden en een verbeterde kwaliteit van leven na de 5 FMT = fecale microbiota transplantaties. Gegeven twee wekelijks in capsules. Waarbij ook de darmflora - darmmicrobioom veranderde en bleef veranderd tot tenminste 1 jaar daarna. 

Hier een grafiek van de deelnemende vrouwen en effecten:



Figure 6 Open-label clinical trial of HC FMT in women with FM

Conclusie van de onderzoekers: 

Het volledige studierapport is gratis in te zien of te downloaden met een opbouw van de muizenstudies tot aan de studie met de 14 vrouwen. Met veel grafieken als ondersteuning en gedetailleerd beschreven hoe de onderzoekers te werk zijn gegaan. Een hele interessante studie m.i..

Cover Image - Neuron, Volume 0, Issue 0

Highlights

Transplanting gut microbiota from women with fibromyalgia into mice induces pain
It also induces immune activation, metabolomic changes, and reduced skin innervation
Gut microbiota promotes pain through several mechanisms

Summary

Fibromyalgia is a prevalent syndrome characterized by widespread pain in the absence of evident tissue injury or pathology, making it one of the most mysterious chronic pain conditions. The composition of the gut microbiota in individuals with fibromyalgia differs from that of healthy controls, but its functional role in the syndrome is unknown. Here, we show that fecal microbiota transplantation from fibromyalgia patients, but not from healthy controls, into germ-free mice induces pain and numerous molecular phenotypes that parallel known changes in fibromyalgia patients, including immune activation and metabolomic profile alterations. Replacing the fibromyalgia microbiota with a healthy microbiota substantially alleviated pain in mice. An open-label trial in women with fibromyalgia (Registry MOH_2021-11-04_010374) showed that transplantation of a healthy microbiota is associated with reduced pain and improved quality of life. We conclude that altered gut microbiota has a role in fibromyalgia pain, highlighting it as a promising target for therapeutic interventions.

Supplemental information (6)


Resource availability

Lead contact

Further information and requests for resources and reagents should be directed to the lead contact, Arkady Khoutorsky (arkady.khoutorsky@mcgill.ca).

Materials availability

This study did not generate new unique reagents.

Data and code availability

All data reported in this paper will be shared by the lead contact upon request. 16S rRNA, WGS, and scRNA-seq data were deposited under the NCBI BioProject accession number PRJNA1029994.

Acknowledgments

This study was supported by the Weston Family Foundation and The Louise and Alan Edwards Foundation to Y.S., A.M., and A.K. The project was also supported by the Israel Ministry of Health Chief Scientist Grant for Pilot Studies to A.M. and the Canadian Institutes of Health Research (CIHR, PJT-191992) to A.K. and Y.S. W.C. was supported by a postdoctoral fellowship from The Louise and Alan Edwards Foundation and the Fonds de recherche du Québec – Santé (FRQS). M.D. was supported by a Canadian Institutes of Health Research postdoctoral fellowship. We thank the McGill Centre for Microbiome Research, Cynthia Faubert, and Anna Jimenez for their help with studies involving germ-free mice.

Author contributions

W.C., Y.S., A.M., and A.K. conceived the project, designed experiments, and supervised the research. W.C. performed behavioral and molecular studies in mice with the help of C.W., N.B., S.T., K.C.L., M. Hooshmandi, C.C., V.H., D.H.-T, V.K., J.F., and N.W. J.Z., J.S.M., I.L.K., N.J.B.B., T.S., B.S., P.S., M.P.-K., E.K., and E.G. assisted with study design and interpretation of results. E.G. and N.J.B.B. performed microbiome analyses. F.W., L.-E.L., and Y.D.K. performed in vivo calcium imaging. S.W., B.T., and I.L.K. performed gut immunophenotyping. M.D., N.S.A., and C.A. assessed visceral sensitivity. M. Haddad, R.H., I.K., T.H., R.L., H.B.-Y., M.P., and A.M. performed a clinical trial in humans and collected samples for mouse FMT. W.C., A.K., E.G., and A.M. had unrestricted access to all data and performed the statistical analyses. W.C., Y.S., A.M., and A.K. wrote the manuscript. All authors reviewed the manuscript and discussed the work.

Declaration of interests

The authors declare no competing interests.

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