Serotonin has direct regulatory role in rheumatoid arthritis, suggests a new study

microscope-275984_1920 copyA new study, reported in The American Journal of Pathology, has found that experimentally-induced rheumatoid arthritis in serotonin-deficient mice is worse than disease reported in controls and that some effects of RA can be reduced by serotonin or the compounds that activate serotonin receptors.

Serotonin, (5-hydroxtryptamine, or 5-HT), a type of chemical that helps relay signals from one area of the brain to another, has been directly implicated for the first time in the pathophysiology of rheumatoid arthritis.

Although it is most commonly known as a neurotransmitter within the central nervous system, this study has pointed to additional important functions of serotonin in the periphery.

In the study, researchers used a mouse model of rheumatoid arthritis known as collagen-induced arthritis (CIA) that produces features similar to that of human rheumatoid arthritis. They compared the effects of CIA in normal mice with those in mice which had been genetically bred with a deficiency of a key enzyme needed for serotonin production in peripheral tissues.

Researchers found that both the number and activity of osteoclasts – a type of bone cell that breaks down bone tissue – were higher in serotonin-deficient mice with arthritis and that more bone resorption was detected both at the affected joints and at remote sites. The serotonin-deficient mice also showed a number of other changes in certain cell-signalling molecules.

Subsequent experiments revealed a direct regulatory role of serotonin in rheumatoid arthritis and these novel data suggest a new therapeutic target that could be important for this disabling disease.

Marie-Christine de Vernejoul of the the Université Paris Diderot, one of the lead-researchers in the study, says, “Our study highlights that 5-HT or 5-HT receptors could represent an exciting prospect to regulate the immune response to rheumatoid arthritis and open new perspectives to improve the therapeutic options for patients.”

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