Neurogenic inflammation pathways (NI)

Neurogenic inflammation pathways represent a complex physiological process where the peripheral nervous system directly triggers inflammatory responses in tissues [1, 15]. This occurs through the release of neuropeptides, such as calcitonin gene-related peptide (CGRP) and substance P, from activated nociceptors (C-fibers and Aδ-fibers) [7, 10]. These mediators act on vascular and immune cells to induce vasodilation, plasma protein extravasation (edema), and mast cell degranulation [6, 13]. This pathway plays a critical role in the pathophysiology of various conditions, most notably migraine, where the trigeminovascular system is activated, as well as chronic pain, asthma, and inflammatory skin diseases like psoriasis [4, 14]. Therapeutic strategies targeting these pathways include CGRP receptor antagonists, monoclonal antibodies against CGRP or its receptor, and triptans which inhibit neuropeptide release [}

Other names

Neurogenic inflammationNICutaneous neurogenic inflammationNeuro-immune-cutaneous system

Inhibition of neuropeptide release (e.g., via 5-HT1B/1D agonism), antagonism of neuropeptide receptors (e.g., CGRP receptor or NK1 receptor), and desensitization of nociceptive ion channels (e.g., TRPV1).