CNS regulation of peripheral inflammation, implications in fibromyalgia?
The central nervous system (CNS = brain and spinal cord) can regulate peripheral inflammation, but the pathways and mechanisms by which it does so remain unclear.
The study summarized below investigates the possibility that the neurotransmitter acetylcholine (ACh) exerts an anti-inflammatory effect via binding to a specific receptor found primarily on the synovial lining of rheumatoid arthritis and osteoarthritis joints.
That possibility is confirmed by observations of reduced pro-inflammatory cytokine activity as a result of such binding.
While the authors suggest that the receptor identified in rheumatoid arthritis and osteoarthritis joints might be a potential target for drug development, I am curious if a similar mechanism might explain the connection between observed neurotransmitter abnormalities seen in fibromyalgia and the persistence of peripheral inflammation.
Acetylcholine regulation of synoviocyte cytokine expression by the alpha7 nicotinic receptor.
Summary of the abstract
OBJECTIVE: The central nervous system can regulate peripheral inflammation, but the neuronal routes from the central nervous system to the peripheral tissue, as well as the messengers, remain poorly defined. One candidate is the cholinergic pathway, which releases acetylcholine (ACh). This neurotransmitter can bind to the alpha7 cholinergic receptor (alpha7R) expressed by nonneuronal cells and reduce inflammation.
To test this possibility, we evaluated the expression of alpha7R and its potential role as a target in rheumatoid arthritis (RA).
RESULTS: Protein and mRNA for alpha7R were demonstrated in RA and osteoarthritis synovium, mainly in the intimal lining. ACh significantly reduced the production of pro-inflammatory mediators. The effect was blocked when the alpha7 receptor was blocked.
CONCLUSION: Alpha7R is a potential therapeutic target for inflammatory diseases.