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Paper Details

The Influence of Cholinergic System on Rheumatoid Arthritis

Mehranfard D* and Hamurtekin E

Journal Title:Open Access Journal of Pharmaceutical Research

Rheumatoid arthritis is one of the most prevalent immune-mediated arthritis and is categorized as a chronic, inflammatory and autoimmune disease, which mainly affects the cartilage, synovial joint, and bone, the causes of which remain unknown. There are different factors playing a role in RA pathophysiology on the molecular level, like Citrullination, Regulatory T cells, Monocytes, Macrophages, Platelet microparticles, and RASFs, which mainly induce inflammation by producing pro-inflammatory cytokines such as IL-8, IL-6, IL-1, and TNF. We have two types of cholinergic systems (CS) in our body, Neuronal CS, in which Acetylcholine (ACh) act as a neurotransmitter and NonNeuronal CS in which ACh act as a local signalling molecule for cellular proliferation and regulation of cellular function including the cells involved in RA inflammation. In light of the recent studies, the links between the CS and cells involved in RA molecular pathophysiology suggest new approaches for controlling RA, which will be discussed further. First, is the stimulation of the vagus nerve, which plays an essential role in the cholinergic anti-inflammatory pathway through its main neurotransmitter ACh resulting in downregulation of TNFα and inhibition of inflammation. The second strategy is stimulation of CAP by selective activation of α7nAChR, which is represented by different types of immune cells, such as T and B-lymphocytes, monocytes, dendritic cells, especially macrophages, and FLS through acetylcholine or its selective agonist resulting in decreased TNF production and reduced inflammation. As we discussed previously ACh is one of the necessary components for cellular proliferation especially in RASFs. Choline transporter-like proteins 1 and 2 are accountable for bringing extracellular choline inside the RASFs, which further will convert to ACh within the cell. Therefore, as the final strategy, we can induce apoptotic cell death in RASFs through preventing choline uptake by CTL1 and CTL2. Blocking of choline uptake through Choline transporter-like proteins 1 and 2, presents a novel target for RA treatment, but further in vivo studies are necessary to examine the role of these transporters as drug targets in RA