Fig. 4

Relevant mechanisms of IBD Sympathetic nerve fibers (SNFs) are increased in UC, leading to an enhanced concentration of CA. Parasympathetic nerve fibers (PNFs) are decreased in UC and CD, resulting in inhibition of the vagus pathway through autonomic-related projection neurons of the PVH to the dorsal motor nucleus of the vagus nerve. This inhibition of the vagus pathway suppresses the secretion of ACh, which promotes increased cytokines and contributes to persistent intestinal inflammation as well as inappropriate responses. Decreased PNFs also occur in CD. Reduction in SNFs in CD lead to increased SP-positive nerve fibers, elevated TRPV1, and reduced CA concentrations. The former promotes the secretion of TNF, IL-1β, IL-6, and IL-8. Elevated TRPV1 contributes to the enhancement of TRPV1-immunorective fibers, which can reduce the threshold of pain via regulation of action potentials production. These processes can enhance visceral hypersensitivity. These factors can work on IBD lesions, form a persistent intestinal inflammatory environment and make patients feel pain