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Tachykinin Antagonists in Asthma and Inflammation
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
The evidence reviewed in this chapter indicates that at several locations of the body a TKergic innervation exists from which peptides of the TK family are released, especially during inflammation and in response to potentially harmful/tissue-threatening stimuli. The released TKs produce a number of powerful biological effects which are proinflammatory or frankly inflammatory; in various viscera, including the airways, a powerful contraction of smooth muscles also occurs. These events, which are receptor-mediated and collectively termed “neurogenic inflammation,” provide a mechanism through which the sensory nervous system contributes to initiation and maintenance of the inflammatory process. The preclinical evidence collected thus far, and reviewed in this chapter, indicates that blockade of neurogenic inflammation can be effectively achieved, in a number of animal models of disease, by occluding postjunctional TK receptors with TK receptor antagonists. From the above, a possible therapeutic usefulness of TK receptor antagonists can be envisaged in diseases as diverse as asthma/bronchial hyperreactivity, psoriasis, rheumatoid arthritis, inflammatory bowel diseases, cystitis, and migraine. This hypothesis is currently under evaluation.
Hormones as Immune Modulating Agents
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Neuropeptides exert a powerful regulatory effect on inflammatory reactions. Proinflammatory neuropeptides, such as SP and CGRP, are released from sensory C nerve fibers in response to a variety of irritants. These mediators induce mast cell discharge, increase the permeability of blood vessels, and also act on smooth muscle elements; resulting in neurogenic inflammation. Neural effector junctions are formed between mast cells and C fibers for close regulatory interaction. Neurogenic inflammation may be regarded as an instant host defence mechanism in response to potentially noxious agents, which can be activated rapidly and does not require specific immune products to initiate. However, neurogenic inflammation may contribute to the pathogenesis of numerous immune diseases, which include allergy, rhinitis, arthritis, and gastrointestinal hypersensitivity [365,394,395].
Neuronal Mechanisms of Cutaneous Blood Flow
Published in Geoffrey Burnstock, Susan G. Griffith, Nonadrenergic Innervation of Blood Vessels, 2019
Fred Lembeck, Margarethe Holzbauer
The purpose of cutaneous vasodilatation in response to a noxious stimulus probably lies in the faster removal by the increased blood flow of toxic exogenous substances that penetrate the skin, or of endogenous substances that mediate inflammation and pain. In addition, increased plasma extravasation enables the removal of larger molecules via the lymphatic system. Vasodilatation and plasma extravasation are predominant in the inital phases of inflammation. Inflammation is a process which proceeds in several phases with the main purpose to repair the damaged tissue. Neurogenic influences during the early stages of inflammation have been suspected for a long time. Many recent observations have shown that antidromic vasodilatation represents at least one of the neuronal mechanisms involved. In consequence, the concept “neurogenic inflammation” was introduced (see Reference 54).
János Szolcsányi and capsaicin research – from the early years to his legacy
Published in Temperature, 2023
● Plasma extravasation in response to antidromic electrical stimulation of sensory nerves (e.g. the saphenous nerve) has been quantified on the basis of tissue deposition of Evans’ blue, a substance known to strongly bind to plasma albumin. The response was apparently not decreased by antagonists acting at muscarinic or nicotinic acetylcholine receptors, some serotonin receptors (methysergide), β- and α-adrenergic, histamine (now: H1) receptors or a cholinesterase inhibitor. Irritant substances like capsaicin, mustard oil (allyl isothiocyanate) and others also elicited plasma extravasation. All these stimuli became largely ineffective after chronic/subacute, but not acute sensory denervation, as well as after systemic desensitization to capsaicin. Thus, neurogenic inflammation is produced by sensory nerves that release a mediator or mediators (whose identity, however, remained unknown).
Capsaicin and cancer: Guilty as charged or innocent until proven guilty?
Published in Temperature, 2023
The neuroimmune regulation of carcinogenesis is subject to excellent recent reviews [108–110]. The diverse roles that capsaicin-sensitive afferents are thought play in neuroimmune interactions are detailed elsewhere [111]. Briefly, capsaicin-sensitive afferents are sites of release for a number of neuropeptides, such as substance P (SP) and calcitonin gene-related peptide (CGRP), that initiate the biochemical cascade known as neurogenic inflammation (Figure 1) [54–56]. Neurogenic inflammation has been implicated in the pathogenesis of various human diseases, including cancer [112]. Sensory neuropeptides also play a role in the regulation of local blood flow [56] that, in turn, may influence cancer growth and metastasis (Figure 3). Last, these neuropeptides may exert trophic actions on tumor cells and/or change their phenotype, rendering the cancer more or less aggressive [113,114]
The Relationship Between Corneal Dendritic Cells, Corneal Nerve Morphology and Tear Inflammatory Mediators and Neuropeptides in Healthy Individuals
Published in Current Eye Research, 2019
Luisa H. Colorado, Maria Markoulli, Katie Edwards
Neurogenic inflammation involves a change in the sensory nerve endings by the release of neuropeptides, because of the activity of inflammatory mediators, modifying the function of sensory neurons.39 Neurogenic inflammation research has been undertaken in disease processes such as arthritis, colitis, bladder inflammation, and asthma.40 In the trigeminovascular system, neuropeptide release further activates trigeminal afferents, inducing sensitization.41 Neuropeptides such as substance P are contained within sensory fibers and these, as well as cytokines, may be released to further modulate inflammatory events.42 The positive associations found in this study between nerve parameters in the avascular central corneal and DC density in healthy subjects supports that the ocular nervous and immune systems are interlinked, specifically in those individuals undergoing presumed immune activity response evidenced by increased number of DCs migration in the central cornea. It is also hypothesized that these correlations change in direction and are stronger and more significant during inflammation. Reduced nerve density and increased DCs has been demonstrated in a dry eye with and without Sjögren syndrome43 and during infectious keratitis,8 with strong negative correlations between these parameters not only in the affected but also the fellow eye,44 indicating a systemic effect.