File:Neuroinflammation of the skin.jpg

Summary

From https://www.mdpi.com/1422-0067/24/5/5001

Figure 1. In the neurogenic inflammatory pathway, peripheral nerve endings communicate with various skin cells, such as keratinocytes, melanocytes, fibroblasts and MCs, and also with immune cells via neurotrophins and neuropeptides. In neurogenic inflammation, an important role is played by MCs, on the surface of which there are numerous receptors for neuropeptides secreted by nerve endings. After activation of the receptors, mast cells degranulate and release proteases, cytokines and histamine. Tryptase binds to the PAR-2 receptor, activating it and releasing neuropeptides such as CGRP and SP, which are responsible for itching and scratching. PAR-2 activation is associated with pain perception. Tryptase directly affects CGRP, causing its degradation and negative feedback. On the other hand, SP, acting on the NK-1R and MRGPRX2 receptors on mast cells, activates them, causes cell degranulation and intensifies the inflammatory response. This response also involves TH2CD4+ immune cells that release cytokines IL-4, IL-13 and IL-31; these cytokines, as mediators, activate receptors on nerve endings, which intensifies itching in skin diseases. Ca2+-dependent TRPV1 and TRPA1 ion channels can communicate with each other and, when activated, increase the release of neuropeptides, thereby exacerbating neurogenic skin inflammation

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