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. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: Gastroenterology. 2020 Feb 19;158(8):2195–2207.e6. doi: 10.1053/j.gastro.2020.02.022

Figure 7. The role of PGE2 produced by colonic mast cells in the pathogenesis of visceral hypersensitivity in IBS.

Figure 7.

Proinflammatory mediators in the mucosa such as histamine, tryptase, among others, are increased in IBS. These mediators, together with histamine and tryptase from MC, activate G protein–coupled receptors (GPCRs) on MC, resulting in degranulation of numerous vesicular mediators (histamine, tryptase, PGE2, etc.) and induction of transcriptional activation of COX2, which increases the synthesis of prostaglandins, including PGE2. MC located close to sensory nerve fibers in the submucosa release PGE2, which acts on sensory fiber EP2 receptors and potentiates the action of pronociceptive mediators released by mechanical or chemical stimulation, leading to the development of VH.