Passive transmission of fibromyalgia symptoms from patient to mouse.

Citation Information: J Clin Invest. 2021;131(13):e144201. https://doi.org/10.1172/JCI144201.

Commentary

Fibromyalgia syndrome (FMS) is an intractable disease in Japan, and this study investigates the characteristics of fibromyalgia and hints for treating it.

Fibromyalgia syndrome causes widespread pain and tenderness, and patients experience chronic fatigue and mental anguish. The etiology and pathophysiology are not fully understood and there is no effective drug treatment.

The results of this study indicate that IgG from FMS patients causes sensory hypersensitivity by sensitizing nociceptive neurons.

The study involved mice treated with IgG from FMS patients, which showed increased sensitivity to mechanical and cold stimuli, and nociceptive fibers in cutaneous nerve specimens showed increased responsiveness to cold, mechanical stimuli.

These mice showed decreased spontaneous locomotion, decreased leg grip strength, and loss of intraepidermal innervation; in contrast, IgG-depleted serum from FMS patients and transfer of IgG from healthy control subjects had no effect.

In addition, IgG from patients did not directly activate naïve sensory neurons.

This result explains why treatment to reduce patients' IgG titers may be effective in fibromyalgia, as IgG from FMS patients sensitizes peripheral nociceptive afferents, causing painful sensory hypersensitivity. This is one of the possibilities for future treatment, but since the subject is not human, caution is needed in interpretation.