Жүйкелік қабыну: механизмдері мен аурулары

Type of 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). 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 and the irritant/wasabi receptor TRPA1. TRPA1 channels stimulated by lipopolysaccharide (LPS) may also cause acute neurogenic inflammation. 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. Neurogenic inflammation appears to play an important role in the pathogenesis of numerous diseases including migraine, psoriasis, asthma, vasomotor rhinitis, fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivity. 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. leading to a "sterile neurogenic inflammation."

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. 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.

In a 2012 article in Nature Neuroscience Chiu et al. discuss the development of science related to neurogenic inflammation and provide a graphic illustrating key discoveries leading toward the current understanding of neurogenic inflammation, its mechanisms, and the conditions caused by its disorder.