Fibromyalgia is a chronic disease that mostly affects women. The persistent muscle and joint pain that characterizes this disease seem to be the work of the brain, but a recent study has explored another avenue: that of autoimmunity.
Fibromyalgia Tender Points
About 2% to 4% of the US population, mostly women, are affected by fibromyalgia, a poorly understood chronic disease characterized by constant muscle and joint pain, general fatigue, sleep disturbances, and poor mental health, prone to anxiety and depression. The constant feeling of pain, exacerbated by cold, stress, or humidity, is associated with the dysfunction of pain circuits in the brain and peripheral nervous system. Some patients also have dysregulation of the immune system.
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The immune track of fibromyalgia has interested Swedish and British researchers. They wondered whether autoantibodies, which attack one’s own body, could play a role in the development of the disease’s main symptoms. They publish the results of their experiments with mice in The Journal Of Clinical Investigation.
Transfering fibromyalgia to mice
The hypothesis presented in this publication is as follows. If autoantibodies, IgG to be precise, play a role in fibromyalgia, healthy mice should develop symptoms of the disease when injected with them. So they were injected with serum from persons with fibromyalgia, which contains only IgG.
The rodents developed the symptoms of fibromyalgia after this injection. They became more sensitive to cold and mechanical stimuli and lost their alertness. In contrast, serums from healthy humans, or those from patients without their IgG, did not make the mice sick.
The link between autoantibodies and pain
How do these autoantibodies work? According to the authors’ findings, they do not activate sensory neurons, but bind, among other things, to glial satellite cells located in the spinal ganglion of the mice. In vitro tests have also shown that these autoantibodies can also bind in humans.
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Autoantibodies isolated from fibromyalgia patients thus sensitize pain receptors in the peripheral nervous system. They become hyperreactive to stimuli and send pain signals to the brain.
Currently, there is no treatment for the cause of fibromyalgia. Treatment is limited to light exercise and antidepressants, but for many patients, this does not work. A better understanding of the role of immunology in this disease could open up new treatment options. Treatments aimed at reducing the amount of IgG in the serum, such as plasmapheresis, could improve the lives of patients who are often at their wit’s end.
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References
Passive transfer of fibromyalgia symptoms from patients to mice
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