Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms of action of prophylactic antiallergic drugs, especially disodium cromoglycate (DSCG), have been reviewed. Some evidence is presented that suggests that DSCG acts not only as an inhibitor of mediator release from mast cells, but also by inhibiting the effects of mediators on bronchial and intestinal smooth muscle. The protective effects of DSCG at these sites can be "ascribed" to the membrane stabilizing effects of this drug on mast cells and smooth muscle fibers, through changes in membrane permeability to calcium and other ions required for mast cell degranulation or smooth muscle contraction. A stabilizing effect on the myenteric plexus also seems to be involved, and can be partially responsible for the beneficial role of this drug in food allergy. Other possible mechanisms of action of prophylactic antiallergic drugs are also discussed in this review.
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PMID:Current views of the mechanism of action of prophylactic antiallergic drugs. 612 70

In a clinical study the participation of histamine in the allergenic response of patients with food allergy was investigated. The resting levels of gastric tissue and plasma histamines of 10 patients were slightly higher than the respective values of normal volunteers. 5 minutes after local intragastral allergenic provocation a decline of the mucosal histamine content of the allergen-treated area was noticed. Parallel investigations on the mast cell content of the stomach mucosa revealed a parallel decrease of the o-phthaldialdehyde stained cells, whereas the number of toluidine blue stained cells remained unchanged. These data are in accordance with an antigen-induced IgE-dependent liberation of the mast cell histamine stores.
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PMID:Release of gastric histamine in patients with urticaria and food allergy. 617 8

Oxatomide is an orally active H1-histamine receptor antagonist which, as appears to occur with some other antihistamines, also inhibits mast cell degranulation. Oxatomide has demonstrated response rates similar to those with other more established members of its drug class in a few studies of chronic urticaria and allergic rhinitis. Interestingly, some patients responding to oxatomide were said to be unresponsive to previously administered antihistamines. The effect of oxatomide was little different from placebo in clinical trials of bronchial asthma in adults. While somewhat more encouraging results have been reported in children with bronchial asthma when higher than presently recommended dosages were employed, and in follicular conjunctivitis, atopic dermatitis and food allergy, reports to date are largely preliminary in nature and additional well-controlled studies are needed to clarify the efficacy of oxatomide in such conditions. The drug has been generally well tolerated, but shares some of the familiar H1-histamine receptor antagonist side effects. As with other similarly acting drugs, the 2 primary side effects with oxatomide are drowsiness and weight gain. Thus, on the basis of present evidence, a trial with oxatomide seems a potentially useful alternative in patients with conditions known or thought to be allergic in nature, in whom more established treatments were ineffective or poorly tolerated.
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PMID:Oxatomide. A review of its pharmacodynamic properties and therapeutic efficacy. 620 Feb 90

Allergic or pseudo-allergic reactions elicited by per os intake of foods, food additives or drugs may be based on one or several of the following immunopathologic mechanisms: 1) specific IgE bound to mast cells and/or basophils; 2) antigen-IgE soluble complexes hitting various target cells; 3) antigen-IgG complexes generating anaphylatoxins; 4) generation of anaphylatoxins by alternate pathway complement activation; 5) release of mast cell mediators by other direct triggering mechanisms (e.g., basic peptides, peptones); 6) effects on other target cells such as neutrophils and platelets; 7) reactions mediated by specific effector lymphocytes. While allergic reactions in a classical sense involve a sensitization process leading to the formation of specific immunologic agents such as antibodies or specific T lymphocytes, pseudo-allergic reactions appear to involve the same inflammatory mediators which are formed and/or released through different mechanisms and without the necessity for specific sensitization. The complexity of the phenomena possibly involved continues to create great difficulties in the objective diagnosis of food allergy.
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PMID:Pathophysiologic mechanisms of allergic and pseudo-allergic reactions to foods, food additives and drugs. 639 Dec 87

Adverse reactions to foods are not infrequent. They may be mediated by immunological mechanisms (food allergy) or non-immunologically (idiosyncrasy, pseudo-allergy, intolerance). Furthermore toxic effects of foods have to be clearly distinguished from food allergy as well as poorly defined conditions such as hyperkinesis or "tension-fatigue syndrome", the causal relation of which to foods is not well established. The diagnosis of food allergy includes convincing history, positive provocation and demonstration of immunological sensitization (mostly IgE, however other types of immune reactions may also be of importance. In the treatment of food allergy specific elimination diets as well as pharmacotherapy with the use of mast cell blocking agents are recommended. In single cases oral hyposensitization may be tried.
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PMID:[Food allergy and other adverse reactions caused by food]. 648 16

Recently, DSCG has been found to inhibit the contraction of guinea pig ileum smooth muscle, when induced by various pharmacologic stimuli. DSCG also seems to inhibit contractions induced by electrical stimuli when high and low frequencies are used. We intend to further clarify our understanding of the sites of action of DSCG by studying its effects on surgically-isolated guinea pig trachea and ileum. Tissue samples were bathed in Krebs solution and suspended at 37 degrees C with 95% O2 and 5% CO2 as proposed by Constantine. Some ileal samples were denervated by the method of Ambache. The isometric contractions of trachea and ileum were measured at basal conditions and after adding cumulative doses of nicotine, histamine, acetyl choline and PG-F2 alpha. The dose response curve for each substance was determined, as were the effects on each curve of DSCG. DSCG significantly inhibited nicotine-induced contractions of guinea pig ileum (nicotine stimulates the intestinal nerve plexus). Histamine and acetyl choline-induced contractions of denervated ileum were also inhibited by DSCG. Contractions of isolated guinea pig trachea secondary to Ach, Hi and PG-F1 alpha were also effectively antagonized. Our results suggest that DSCG acts at two levels to inhibit ileal contraction: at the neural level, namely at Auerbach's plexus, and directly upon the smooth muscle fiber. These effects probably depend on the membrane stabilizing capability of cromolym sodium, that not only involve the mast cell, but extend to intestinal and bronchial smooth muscle as well. The action of DSCG on smooth muscle and mast cells probably contribute to its efficacy in bronchial asthma and food allergy.
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PMID:Effects of disodium cromoglycate on smooth muscle. 681 51

Nasal secretion samples from 473 children aged 0--15 years were studied in order to evaluate the role of mast cells in the nasal smear in different types of atopy and food allergy. The occurrence of eosinophils in the nasal secretion and in the blood, and susceptibility to upper respiratory infection were recorded. A mast cell count of more than 20 cells per slide was indicative of atopy and there was a clear correlation between eosinophilia and mastocytosis in the nasal smear. No type of allergy seemed to be significantly predominant in the total material, but in young children aged 0--3 years mastocytosis was clearly related to food allergy. The examination of nasal smears for mast cells is a valuable test in diagnosing atopy in children and especially food allergy among young children. However, the test is not reliable enough to be used as a single screening test.
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PMID:Children's atopy and mastocytosis in the nasal smear. 731 9

Adverse reactions to food may, in some cases, be due to IgE-mediated immune reactions to the ingested antigens. A mast cell protector has been shown to protect patients against challenge with food to which they are sensitive. An IgE-mediated intestinal anaphylaxis reaction in the rat has been developed as a model of some aspects of human food allergy. Using this model, a number of xanthones and other anti-inflammatory agents were tested for activity in inhibiting intestinal anaphylaxis. The compounds were also tested for inhibitory activity against the IgE-mediated rat passive cutaneous anaphylaxis reactions. The xanthones protected against both reactions, as did isoproterenol and cyproheptadine, while aspirin, indomethacin, and dexamethasone inhibited the intestinal but not the cutaneous reaction. This suggests that while IgE-triggered mediator release from mast cells is important in both reactions, other mechanisms may also be operative in the intestinal reaction. Furthermore, the use of xanthones and other anti-inflammatory compounds may be a useful mode of therapy in human food allergy.
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PMID:Inhibition of rat intestinal anaphylaxis by various anti-inflammatory agents. 740 52

In 100 dogs with 4 inflammatory dermatologic diseases, buffy coat preparations from EDTA-treated blood samples were examined cytologically. Fifty-four dogs had atopy, 26 had flea-bite hypersensitivity, 17 had sarcoptic mange, and 3 had food allergy. Twenty-eight dogs had 2 or more concurrent skin diseases; most of these had secondary pyoderma. Dogs did not have mast cell tumors. Thirteen samples contained 1 or more mast cells/4 slides reviewed. This study revealed that dogs with inflammatory skin diseases can have a few to many mast cells evident on cytologic examination of buffy coat preparations.
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PMID:Identification of mast cells in buffy coat preparations from dogs with inflammatory skin diseases. 775 Dec 39

This study was undertaken to investigate the kinetics of histamine and tryptase in the circulation of patients with food allergy and to determine whether the measurements of plasma histamine and tryptase concentrations after food challenges provided additional predictive markers for the diagnosis and evaluation of food allergy. Twenty-one open food challenges were performed on 13 patients with suspected food allergy. Plasma histamine and tryptase concentrations were measured during 4 hours after challenge. In the group of patients with immediate reactions after challenges, the mean plasma histamine concentration rose significantly at 120 and 240 minutes after the challenge, and the mean plasma tryptase concentration was increased significantly at 240 minutes after challenge. Plasma histamine and tryptase concentrations were measured during 24 hours after 8 open food challenges in 7 other patients with suspected food allergy. In each patient with a nonimmediate reaction, plasma histamine concentrations were increased at the onset of symptoms after challenge, but no plasma tryptase concentrations increased. The elevation of plasma histamine and tryptase in patients with immediate reactions following food challenge indicates mast cell activation. On the other hand, the elevation of plasma histamine without elevated plasma tryptase in the patients with nonimmediate reactions following food challenge may indicate basophil activation rather than mast cell activation. Plasma histamine and tryptase measurements after food challenge may be useful in the detection and evaluation of food allergy.
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PMID:Time course of plasma histamine and tryptase following food challenges in children with suspected food allergy. 834 67


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