Plain Language Summary of Fibromyalgia Study
Titre de l'article: Transfert passif des symptômes de la fibromyalgie des patients aux souris
Date de publication 2021
Référence de la revue Goebel A et al. J Clin Invest 2021;131(13):e144201. (Open Access)
Contexte
The cause/s of fibromyalgia(FM) is not completely understood.
Why this Study
In the general population the incidence of FM is at least 2% but increases to 10-30% in people who have autoimmune rheumatological conditions. Based on this increase in prevalence the authors investigated whether autoreactive IgG is responsible for some of the key symptoms in FM. IgG is a type of protein antibody found in the blood, which protects us from bacterial and viral infections.
Qui a participé à l'étude ?
FM patients and healthy controls and mice. The numbers of human’s used to obtain IgG (FM or non-FM) and mice varied depending on the test performed. Numbers varied from 6-8 humans to 39-44 humans and 6-12 mice.
Comment l'étude a-t-elle été menée ?
The human blood samples provided purified serum IgG. This IgG was injected into mice.
The researchers did four main things:
- They checked if the mice acted like they were in pain after getting the IgG.
- They looked at specific nerves in the mice to see if they became more sensitive.
- They used special tests to see where the IgG ended up in the mice.
- They looked at how the IgG changed the nerves in the skin of the mice.
Résultats
Several key FM features can be induced in mice injected with IgG from human FM patients (tenderness and hypersensitivities to heat and cold variabilities). In addition, a decrease in grip strength and spontaneous locomotor activity was induced.
Limites de l'étude
Limited numbers of humans and mice used.
Conclusions
IgG may play a role in the underlying cause of FM. Future studies are needed to look into the cellular and molecular mechanisms for IgG-mediated FM symptoms. Future studies are needed to investigate therapies that decrease IgG levels in FM patients as possible treatments. Also, to investigate treatments that interfere with the binding of autoreactive antibodies or prevent the consequences of these autoantibodies.
Article summarized by FAC Research Committee September, 2023
For more information consult the original article
https://pubmed.ncbi.nlm.nih.gov/34196305/
