Neurogenic inflammation

Neurogenic inflammation is a process in which sensory nerve fibers (primarily nociceptors) release neuropeptides such as substance P, calcitonin gene-related peptide (CGRP), and neurokinin A in response to noxious stimuli or tissue injury[1][3][5][7]. These neuropeptides act on neighboring blood vessels and immune cells to induce vasodilation, increase vascular permeability (causing edema), and recruit immune cells, leading to the signs and symptoms of inflammation[1][3][5]. Central channels implicated in this process include transient receptor potential ion channels TRPV1 and TRPA1[1][5][7]. Neurogenic inflammation is implicated in the pathogenesis of various disorders, including migraine, psoriasis, fibromyalgia, asthma, vascular and dermatological conditions, and some autoimmune and allergic diseases[1][3][5][7]. While it is an important mechanism underpinning pain and tissue response, **neurogenic inflammation itself is not a molecule, protein, or receptor, but a network phenomenon involving multiple interacting targets**[1][3][7]. For therapeutic intervention, the actual targets are often specific neuropeptide receptors or ion channels (such as NK-1 receptor, TRPV1, CGRP receptor, etc.) rather than neurogenic inflammation as a process[4][5][7]. In summary, "Neurogenic inflammation" is not a canonical drug target, but a descriptive term for a biological process; therefore, using it as a molecular or receptor target is incorrect.