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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mechanism of inhibition of mast cell anaphylaxis by P. kurroa-extract (PK) treatment in rats was investigated. Mast cell-IgE binding, assessed from induction of passive sensitization, was not affected. Calcium-independent early activation events in mast cell anaphylaxis indicated on inhibitory influence of PK-treatment. Inhibition of membrane-protease release by PK-treatment was suggested by study of gastric secretion and exhibition of saturable synergism with Di-isopropyl fluoro phosphate on inhibition of anaphylactic degranulation. pH-independence of mast cell stabilizing effect negates any PK-influence on phospholipid transmethylation. The results complement findings of earlier studies on indirect effects of PK through alteration of membrane structure/function.
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PMID:Immunopharmacological studies on Picrorhiza kurroa Royle ex Benth. Part VI: Effect on anaphylactic activation events in rat peritoneal mast cells. 266 36

The authors report the case of a 12 year-old boy with exercise-induced anaphylaxis. Angioedema was the main symptom and was accentuated by ingestion of an orange prior to exercise. Exercise-induced anaphylaxis is due to mast cell degranulation that is triggered by exercise alone or, less commonly, by the combination of a sensitizing food and exercise. The symptoms of exercise-induced anaphylaxis may be moderate or severe, with laryngeal dyspnea and shock. Prevention is based on avoidance of the offending food before exercise and a reduction of the intensity (and even the suppression) of exertion.
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PMID:[Anaphylaxis syndrome induced by exercise]. 266 84

A diagrammatic representation of the interactions between mediators of hypersensitivity and leukocytes in early, late-phase, and ongoing asthma is shown in Figure 1. Early phase or immediate reactions are largely the result of bronchoconstriction consequent to the release of mediators such as histamine, PGD2, LTC4/D4, and PAF. The principal mediator cell (MC) is the mast cell (although other IgE receptor-bearing cells such as the macrophage, eosinophil, and platelet might also be involved in this immediate response). The stimulus for mediator cell activation may be either immunologic (IgE-dependent) or nonimmunologic (i.e., changes in osmolarity as a result of the respiratory water loss associated with exercise-induced asthma). Late-phase reactions appear to be a consequence of infiltration with neutrophils (N), eosinophils (E), and macrophages (M phi). These cells are recruited and activated either by mast cell-associated chemotactic factors [such as LTB4, PAF, the eosinophil chemotactic factor of anaphylaxis (ECF-A), or high-molecular weight neutrophil chemotactic activity (NCA (HMW))] and/or "lymphokines" derived from T-helper cells (TH) which have been stimulated by antigen processed by the antigen-processing cells (APC). These mononuclear cell interactions are under the control of regulatory T cells [T suppressor (TS) cells] and it is speculated that the availability of these subsets may determine the magnitude of the late-phase response. Lymphokines and monokines which selectively activate neutrophils, eosinophils, and monocytes include LIF, EAF, and IFN-gamma, respectively. Macrophage-derived tumor necrosis factor (TNF) also amplifies the inflammatory response by its capacity to enhance eosinophil cytotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inflammatory cells in bronchial asthma. 270 38

We used genetically mast cell-deficient WBB6F1-W/Wv and WCB6F1-S1/S1d mice and the congenic normal (+/+) mice to investigate the effects of intravenous infusion of goat antimouse IgE on heart rate (HR), pulmonary dynamic compliance (Cdyn), pulmonary conductance (GL), and survival. In WBB6F1-+/+ and WCB6F1-+/+ mice, anti-IgE induced extensive degranulation of tracheobronchial mast cells, as well as significant elevation of HR, significant reductions in Cdyn and GL and, in some cases, death. In contrast, W/Wv and S1/S1d mice exhibited little or no pathophysiological responses and no mortality after challenge with anti-IgE. In W/Wv mice reconstituted with mast cells by intravenous administration of bone marrow cells derived from congenic +/+ mice (+/+ BM----W/Wv mice), anti-IgE induced extensive mast cell degranulation, as well as pathophysiological responses and mortality similar to those observed in WBB6F1-+/+ mice. These findings suggest a critical role for mast cells in the development of the cardiopulmonary changes and mortality associated with anti-IgE-induced anaphylaxis.
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PMID:Role of mast cells in anaphylaxis. Evidence for the importance of mast cells in the cardiopulmonary alterations and death induced by anti-IgE in mice. 278 2

Intracutaneous injection of purified peritoneal macrophages harvested from ovalbumin (OVA)-hypersensitive high-IgE-responder BN rats into naive animals sensitised the injection sites for subsequent OVA-specific passive cutaneous anaphylaxis (PCA) reactions. The underlying mechanism(s) were investigated using a macrophage cell line (WEHI 265.1), which exhibited comparable sensitising activity in rat or mouse skin, after initial pulsing in vitro with antiserum rich in OVA-specific IgE. Transfer of OVA-hypersensitivity by the cell line (1) was IgE-dependent and did not occur when the cells were pre-exposed to antiserum containing OVA-specific IgG alone, (2) was blockable by saturation of cell surface receptors in the recipient with myeloma IgE (but not myeloma IgG), and (3) did not occur in mast cell-deficient mice carrying the W/Wv mutation, in contrast to their normal heterozygous littermates which developed marked OVA-hypersensitivity at the injection site. These results are consistent with arming of IgE-receptors on cutaneous mast cells by IgE antibody released from macrophages, and hint at a possible role for phagocytes in amplifying IgE-mediated reactions in tissues.
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PMID:In vivo arming of cutaneous mast cell receptors by IgE released from macrophages. 279 24

New 1-(2-pyridinyl)piperazine derivatives were synthesized and tested as inhibitors of the reaginic passive cutaneous anaphylaxis in the rat (PCA), of the histamine-induced bronchospasm in the guinea pig, and of the rat mesenteric mast cell degranulation induced by compound 48/80. On the basis of test results, a series of N-(substituted phenyl)-omega-[4-(2-pyridinyl)-1-piperazinyl]alkanamides was prepared. The nature of substituents at the anilide ring strongly influenced mast cell stabilizing activity, whereas it was less determining in the case of the other two tests. No clear correlation between the most common physicochemical parameters (pi, sigma, Vw volume) of substituents and activity could be detected. With regard to the position of substituents at the anilide ring, the rank order of potency, in the PCA and bronchoconstriction tests, was para greater than meta greater than ortho. Introduction of substituents in the 1-(2-pyridinyl)piperazinyl moiety of the N-(substituted phenyl)propanamide derivatives hardly affected activity, or the effect was deleterious. Some of the new compounds exhibited a simultaneous remarkable activity in all the three assays employed.
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PMID:1-(2-pyridinyl)piperazine derivatives with antianaphylactic, antibronchospastic, and mast cell stabilizing activities. 287 15

The mechanism(s) of adverse reactions to sulfites remains unclear. To determine whether mast cell degranulation is involved in sulfite sensitivity, we performed single-blind, placebo-controlled oral aqueous challenges with potassium metabisulfite in 13 patients with histories suggestive of sulfite sensitivity. Ten patients were also skin tested with potassium metabisulfite at 10 mg/mL and all had negative reactions. Serum samples were obtained from all the patients before the challenge and for 180 minutes after the challenge. The samples were tested for the presence of neutrophil chemotactic factor of anaphylaxis, using both a 51chromium microchamber chemotaxis assay and a leukocyte polarization technique. Six of 13 patients had positive challenges as defined by a fall equal to or greater than 20% in their forced expiratory volume in one second. No significant increase in neutrophil chemotactic factor activity was detected in the postchallenge serum samples from patients who experienced positive or negative challenges. We conclude that sensitivity to aqueous metabisulfite is not associated with mast cell degranulation in metabisulfite skin test-negative patients.
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PMID:Studies of neutrophil chemotactic factor of anaphylaxis in metabisulfite sensitivity. 291 98

Antigenic challenge of jejunum from rats infected with Trichinella spiralis evokes a biphasic pattern of epithelial Cl- secretion, as measured in vitro by electrophysiological methods. Peaks of secretion occur at approximately 1.5 and approximately 5.0 min post-challenge. Challenge of jejunum from hosts passively immunized with serum containing anti-Trichinella anaphylactic antibody evokes the late phase but not the early phase of Cl- secretion. Since the early phase is mediated by 5-hydroxytryptamine and histamine from mast cells, we hypothesized that the failure to express that phase was due to a decrease in mast cell-derived mediators secondary to a deficiency in mucosal mast cell numbers. The hypothesis was tested by correlating mast cell numbers with patterns of antigen-induced Cl- secretion using several immunization regimes. Rats actively immunized by infection produced anti-Trichinella IgE and had a mucosal mastocytosis. Rats passively sensitized with serum containing anti-Trichinella IgE had normal numbers of mast cells in their mucosa. Inducing mastocytosis in rats, by infecting them with Nippostrongylus brasiliensis prior to passive sensitization with anti-Trichinella serum, primed for the expression of a biphasic Cl- secretory response upon subsequent challenge with Trichinella antigen. Rats actively sensitized by injection with Trichinella antigen elicited an IgE response without mastocytosis and expressed only the late phase of antigen-induced Cl- secretion. Results (i) support our hypothesis, (ii) emphasize the importance of the cellular state of the mucosa in the functional expression of local anaphylaxis; and (iii) provide a physiological explanation for the general failure of vaccination and passive sensitization to induce functional immunity equivalent to that induced by natural infection.
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PMID:Simulation of parasite-induced gut hypersensitivity: implications for vaccination. 292 27

It has been suggested that patients with recurrent, unexplained anaphylaxis may be more responsive, and patients with systemic mastocytosis, less responsive, to mast cell-derived mediators, including histamine, compared to normal subjects. This would help explain why patients with recurrent, unexplained anaphylaxis have an anaphylactic response and, conversely, why patients with systemic mastocytosis can tolerate high levels of plasma histamine. To test this hypothesis, intradermal titrations (0.02 ml of solution from 1 ng/ml to 2 micrograms/ml) of histamine and morphine sulfate (MS) (10 ng/ml to 10 micrograms/ml) were administered to normal volunteers (N = 15), patients with recurrent, unexplained anaphylaxis (N = 10), and patients with systemic mastocytosis (N = 18). Antihistamines were stopped at least 72 hours before the study. Resultant areas of wheal and flare were determined with a computerized morphometric system. Comparison of any two given means at each dose of histamine or morphine with the two-sample Student's t test with Bonferroni inequality demonstrated no significant differences (p greater than 0.05) among the three groups. The median amount of MS or histamine required to produce a half-maximal response was compared for equality. None of the differences observed reached statistical significance, in agreement with the similarity of the dose-response curves. An analysis of the correlation between response to MS and to histamine in individual subjects revealed the responses to be significantly correlated in all cases, with the exception of wheal in patients with recurrent, unexplained anaphylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of the wheal-and-flare reactions that follow the intradermal injection of histamine and morphine in adults with recurrent, unexplained anaphylaxis and systemic mastocytosis. 292 81

The gene for a human epsilon chain Fc fragment has been cloned and expressed at a high level in Escherichia coli, and its biological activity in binding to the high-affinity receptors on mast cells and basophils and mediating histamine release has been examined in a variety of assays, including the inhibition of passive cutaneous anaphylaxis in human skin, which was induced by ragweed immunoglobulin IgE antibody and antigen. The positive results obtained in these assays encouraged us to try to analyse the binding site on IgE by site-directed mutagenesis. We describe deletion mutants here that narrow down the binding site on IgE for the mast cell receptor to a stretch of 76 amino acids (residues 301-376 on the ND epsilon chain) spanning the CH2 and CH3 domains. This peptide displays activity in the human skin test indistinguishable from that of a myeloma IgE.
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PMID:Recombinant human IgE. 295 1


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