Neurogenic inflammation

Neurogenic inflammation is inflammation arising from the local release by afferent neurons of inflammatory mediators such as Substance P, Calcitonin Gene-Related Peptide (CGRP), neurokinin A (NKA), and endothelin-3 (ET-3).[1][2][3] In such neurons, release of these pro-inflammatory mediators is thought to be triggered by the activation of ion channels that are the principal detectors of noxious environmental stimuli. In particular, the heat/capsaicin receptor TRPV1[4] and the irritant/wasabi receptor TRPA1.[5][6][7] TRPA1 channels stimulated by lipopolysaccharide (LPS) may also cause acute neurogenic inflammation.[8] Once released, these neuropeptides induce the release of histamine from adjacent mast cells. In turn, histamine evokes the release of substance P and calcitonin gene-related peptide; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established.[9]

Neurogenic inflammation appears to play an important role in the pathogenesis of numerous diseases including migraine,[10][1][11][12] psoriasis,[2][13][14] asthma,[15] vasomotor rhinitis,[16] fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivity. [17][18][19]

In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via release of neuropeptides including Substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, Neurokinin A and CGRP.[20][21] leading to a "sterile neurogenic inflammation."[22]

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