Neurogenic inflammation
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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] For example, release of neuropeptides can increase vasodilatation and capillary permeability of vascular endothelial and smooth muscle cells.[4]
The release of pro-inflammatory mediators is thought to be triggered by the activation of ion channels that are the principal detectors of noxious environmental stimuli. The heat/capsaicin receptor TRPV1[5] and the wasabi receptor TRPA1.[6][7][8] TRPA1 channels stimulated by lipopolysaccharides may also cause acute neurogenic inflammation.[9]
Once released, these neuropeptides induce the release of histamine from nearby mast cells. In turn, histamine evokes the release of substance P and CGRP; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established.[10]
Neurogenic inflammation appears to play a role in the pathogenesis of numerous disorders, including migraine,[11][4] psoriasis,[2] asthma,[12] vasomotor rhinitis,[13] fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivity.[14][15][16] In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via the release of neuropeptides, including substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, neurokinin A, and CGRP.[4]
Magnesium deficiency causes neurogenic inflammation in a rat model. Researchers have theorized that since substance P which appears at day five of induced magnesium deficiency, is known to stimulate in turn the production of other inflammatory cytokines including IL-1, Interleukin 6 (IL-6), and TNF-alpha (TNFα), which begin a sharp rise at day 12, substance P is a key in the path from magnesium deficiency to the subsequent cascade of neuro-inflammation.[17] In a later study, researchers provided rats dietary levels of magnesium that were reduced but still within the range of dietary intake found in the human population, and observed an increase in substance P, TNF alpha (TNFα) and Interleukin-1 beta (IL-1β), followed by exacerbated bone loss. These and other data suggest that deficient dietary magnesium intake, even at levels not uncommon in humans, may trigger neurogenic inflammation and lead to an increased risk of osteoporosis.[18]