Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cutaneous wheal and flare responses to increasing concentrations of calcitonin gene-related peptide, substance P, neurokinin A, vasoactive intestinal polypeptide (VIP), compound 48/80, and phosphate-buffered saline were measured in 10 patients with chronic idiopathic urticaria and 10 healthy controls. A significant increase in VIP-induced wheal, but not flare or cutaneous blood flow, was seen in urticarial patients compared with controls (p less than 0.001). No significant differences in responses to other tested compounds were found between these groups. These data point to an increased sensitivity of microvasculature to VIP in patients with chronic idiopathic urticaria.
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PMID:Cutaneous responses to vasoactive intestinal polypeptide in chronic idiopathic urticaria. 137 Feb 36

Substance P is a decapeptide which forms part of the group known as neuropeptides, that is, peptides released by some neurones such as the slow-conducting C fibres and the rapid-conducting A-delta fibres. These neurones belong to the category of non-adrenergic non-cholinergic nerves (NANC), which perform their action through a mechanism known as "axonic reflex". This mechanism is an antidromic stimulation which produces a secretion of neuropeptides, especially substance P. It is known that substance P, once released, is able to exert a number of actions including among others inflammatory and bronchospastic activities and a stimulation of the immunologic system. Other effects attributed to this substance are an increase in capillary permeability and oedema and the perpetuation of certain conditions such as asthma, rhinitis and chronic urticaria or hives. The production, metabolism and actions of this neuropeptide are described.
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PMID:[Substance P: immuno-allergic implications]. 138 Jul 67

The presence of immunologic markers for neurofilaments, neuropeptides of sensory nerve fibers (Calcitonin gene-related peptide and substance P), for noradrenergic innervation (neuropeptide Y and Tyrosine hydroxylase), and Neuron-specific protein 9.5 was evaluated in frozen tissue sections from normal skin (n = 34) and from skin biopsies manifesting urticaria (n = 6), leukocytoclastic vasculitis (n = 4), systemic lupus erythematosus (n = 23), and atopic dermatitis (n = 40, of which 16 were from lesions induced by epicutaneous atopic allergen patch tests). In some normal skin specimens immunoreactive nerve fibers expressing Neuron-specific protein 9.5 were observed in the epidermis, dermis, and around blood vessels. For the other markers, immunolabeling was mainly observed in the dermis around blood vessels. Neurofilaments, which are scarce in normal skin epidermis, were present in higher density in the epidermis of affected skin in all disease conditions. Biopsies from urticaria and systemic lupus erythematosus showed a decrease in density of fibers immunolabeled for neuropeptides substance P and Calcitonin gene-related peptide and for Neuropeptide Y. In biopsies from skin with atopic dermatitis, an increased density of fibers was observed for all markers except Neuropeptide Y and Tyrosine hydroxylase. In this group, biopsies from positive atopic allergen patch tests showed an enhanced density of fibers labeled by antibody to Neuron-specific protein 9.5 and a lower density in labeling for Tyrosine hydroxylase. The data indicate a potential role of innervation and neuropeptides in dermatoses like atopic dermatitis.
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PMID:Increased number of immunoreactive nerve fibers in atopic dermatitis. 138 6

The role of substance P (SP) in allergic reactions of the skin was investigated. Spantide, a competitive inhibitor of SP, was injected intracutaneously into the volar aspect of the forearm prior to the following challenges: benzalkonium chloride (irritant delayed reaction), tuberculin (immunological delayed reaction), UVB irradiation, benzoic acid (non-immunological contact urticaria), different food allergens and latex (in patients with immunological contact urticaria). Only the immunological reactions of contact urticaria and the reaction to tuberculin were suppressed by the SP antagonist, indicating that SP is involved in their pathogenesis.
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PMID:Substance P antagonist inhibits immediate and delayed type cutaneous hypersensitivity reactions. 172 11

In the present experiments the role of unmyelinated sensory fibres in the mechanism of cutaneous inflammatory reactions under normal and pathological conditions has been studied in man and animals. Dye leakage responses to histamine, serotonin, compound 48/80, bradykinin and substance P were significantly reduced, while neurogenic inflammation was completely abolished in rats treated neonatally with capsaicin, as studied quantitatively by the Evans blue technique. Neurogenic inflammation could also be elicited by mustard oil in normally innervated human skin, but not in skin areas affected by herpes zoster or in a patient suffering from congenital analgesia. Repeated topical treatment of the skin with capsaicin (local desensitization) abolished the neurogenic inflammatory response for several days. Chemical pain sensitivity was strongly reduced, and thresholds for warmth and heat pain sensations were significantly elevated. Local capsaicin desensitization of the skin prevented whealing, flare and itch in patients with acquired cold and heat urticaria. The findings indicate that peptide-containing sensory nerves are involved in the mediation of chemogenic and heat pain, and possibly itch, and are responsible for initiation of the neurogenic inflammatory response. The results also provide direct evidence of the involvement of these particular sensory nerves in the modulation of the permeability-increasing effects of putative mediators of acute inflammatory reactions. It is concluded that, through modulation of cutaneous vascular reactions, peptidergic sensory nerves may play a hitherto unrecognized role in the pathomechanism of certain diseases of human skin.
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PMID:The modulation of cutaneous inflammatory reactions by peptide-containing sensory nerves. 241 73

Topical application of capsaicin is thought to deplete substance P from local sensory nerve terminals. In experiments on human skin inflammation was induced by injection of substance P (SP) or histamine intradermally, UV irradiation, non-immunologic contact urticaria, tuberculin reaction, contact allergens and benzalkonium chloride with or without capsaicin pretreatment. The flare response to SP and histamine was suppressed by capsaicin pretreatment whereas the wheal was enlarged. Interestingly, capsaicin pretreatment enhanced the responses to all other inflammatory agents.
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PMID:The effect of capsaicin on some experimental inflammations in human skin. 243 72

Substance P (SP), calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP) were assayed in lesions and normal skin of patients with dermographism and cold urticaria utilizing suction-induced blisters. There was no difference in SP and VIP concentrations between challenged and control skin of urticaria patients. On the whole, however, the concentration of both neuropeptides, and VIP in particular, was higher in the urticaria patients than in control subjects. CGRP levels were not increased. SP and VIP in blood samples from veins draining challenged skin areas were below the detection limit. It is concluded that SP and VIP may potentiate histamine in wheal formation and thus contribute to the increased reactivity of the skin to trauma and temperature changes in patients with physical urticaria.
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PMID:Occurrence of substance P, vasoactive intestinal peptide, and calcitonin gene-related peptide in dermographism and cold urticaria. 244 38

This short review examines two examples of studies into the mechanisms of allergic responses which have particular relevance to inflammation research. The first is the ability of human skin mast cells, but not those derived from lung, adenoids, tonsils or intestine, to release histamine in response to stimulation by neuropeptides including substance P, vasoactive intestinal polypeptide (VIP) and somatostatin. The neuropeptide activation site does not appear to be a classical tachykinin receptor but rather a binding site of low affinity and low specificity capable of interacting with neuropeptides and compounds with similar physicochemical characteristics. In contrast to IgE-dependent activation, neuropeptide stimulation of skin mast cells induces a rapid release of histamine with minimal generation of PGD2 and LTC4. This pseudo-allergic reaction is thought to underlie the weal and flare response in the skin and may have a role in urticaria. The second example describes studies to elucidate the mechanisms of the late asthmatic response by use of a guinea-pig model. As in man, both early and late phase responses in the guinea-pig are inhibited by sodium cromoglycate whereas only the early response is inhibited by the beta-adrenoceptor stimulant drug salbutamol. Examination of bronchoalveolar fluid has shown a temporal relationship between an airways neutrophilia and the late response. However, pharmacological manipulation and the use of an anti-neutrophil serum has shown that these events are not interdependent. The role of the airways eosinophilia requires further investigation.
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PMID:Allergy or inflammation? From neuropeptide stimulation of human skin mast cells to studies on the mechanism of the late asthmatic response. 265 5

The mechanism(s) by which repeated cold challenge in a patient with idiopathic acquired cold urticaria resulted in the induction of clinical tolerance to cold stimuli was studied. Plasma histamine levels, mast cell ultrastructure, and the cutaneous response to intradermal injections of morphine, histamine, and substance P were examined before and after the induction of tolerance. Plasma histamine levels draining cold-challenged, clinically tolerant skin were markedly diminished compared to histamine levels obtained during cold-induced angioedema. Furthermore, electronmicroscopy of skin samples taken from tolerant skin after cold challenge revealed intact, largely normal appearing mast cells. Intradermal injection of mast cell secretagogues and vasoactive agonists into normal and tolerant skin sites resulted in similar whealing responses. Thus, these studies suggest that the state of clinical tolerance to cold stimuli is due neither to mast cell-mediator depletion or tachyphylaxis of the cutaneous vasculature to vasoactive agonists. It appears likely that tolerance may be due to the induction of a specific state of unresponsiveness of mast cells to cold stimuli or possibly to depletion of a cold-induced cutaneous antigen capable of triggering mast cell degranulation.
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PMID:A case study on the induction of clinical tolerance in cold urticaria. 340 65

A patient with solar urticaria induced by wavelengths 290-420 nm is reported. Wheals appeared after a few seconds of exposure to the sun; longer exposure caused general malaise and syncope. Intradermal injection of in vitro irradiated plasma caused a local whealing which was not seen with plasma kept dark. The wheals induced by irradiation could be inhibited by local injection of an antihistamine. Local injection of lidocaine and hydrocortisone was ineffective. Depletion of substance P in the skin by topical application of capsaicin did not change the sensitivity to irradiation with 313 nm and a single PUVA treatment did not change the minimal urticarial dose (MUD). Sunscreens were in practice of limited value with the exception of a protective plastic helmet. Repeated daily irradiation with UVA in increasing doses normalized his response to sunlight.
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PMID:Solar urticaria: mechanism and treatment. 374 56


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