Abstract
Familial Mediterranean fever (FMF) is a monogenic autoinflammatory disease characterized by recurrent episodes of fever and serositis. Colchicine (Col) has a crucial role in the prevention of amyloidosis and FMF attacks. The effect of Col on innate immune cells is based on the inhibition of the microtubule system. The microtubule system is also very important for neurosecretory functions. The inhibitory effect of Col on neurosecretory functions is an overlooked issue. Considering that the neuroimmune cross-talk process plays a role in the development of inflammatory diseases, the effect of Col on the neuronal system becomes important. FMF attacks are related to emotional stress. Therefore, the effect of Col on stress mediators is taken into consideration. In this hypothetical review, we discuss the possible effects of Col on the central nervous systems (CNS) and peripheral nervous systems (PNS) in light of mostly experimental study findings using animal models. Studies to be carried out on this subject will shed light on the pathogenesis of FMF attacks and the other possible mechanisms of action of Col apart from the anti-inflammatory features.
Highlights
Familial Mediterranean fever (FMF) is a common, Mendelian-inherited monogenic autoinflammatory disease characterized by irregular attacks of paroxysmal fever and serositis [1]
The same investigators found that dopamine beta-hydroxylase (DBH) activity was higher in untreated attack-free patients and patients with attacks than in healthy controls. They have shown that Col reduced DBH activity [75]. These results suggest that the sympathoadrenal system may have a role in the pathogenesis of FMF and that Col interferes with this process
It is reasonable that the future will bring new ways of neuromodulator therapy to target diseases currently treated with drugs [81]
Summary
Familial Mediterranean fever (FMF) is a common, Mendelian-inherited monogenic autoinflammatory disease characterized by irregular attacks of paroxysmal fever and serositis [1]. In contrast to the abovementioned study, Col increased proinflammatory gene expression in vitro in neutrophils and showed its anti-inflammatory effect only through the inhibition of CASP-1 activation [8]. These observations suggest the requirement of another explanation of why Col is ineffective when given during an FMF attack. When the test was repeated after Col was given to the experimental animals, the release of both mediators was completely inhibited Such an inhibitory effect of Col has been reported in various types of secretions: insulin [61], histamine from mast cells [62], and collagen from osteoblasts [63, 64]. Col blocks pro-inflammatory cascades by inhibiting the activation of purinergic receptors P2X2 and P2X7 [80] (Table 1)
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