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

The activation of mast cells by immunologic or physical stimuli leads to the generation of unstored intermediates (mediators) such as slow reacting substance of anaphylaxis (SRS-A) and platelet activating factor (PAF), and to their release along with performed mediators, histamine, eosinophil chemotactic factor of anaphylaxis (ECF-A), and neutrophil chemotactic factor (NCE), and macromolecular heparin. The internal regulation of mast cell-dependent phenomenons occurs at at least four levels: 1) the intensity and nature of the activating stimulus, 2) the regulation of mediator generation and release of cellular levels of the cyclic nucleotides, 3) the capacity of target cells to bind and respond to primary mediators, and 4) the rate at which mediators undergo biodegradation. Inasmuch as the mast cell is present at cutaneous and mucosal surfaces about venules, it seems likely that the initial or humoral phase of its response achieves an influx of plasms proteins, such as immunoglobulins and complement components, whereas the subsequent cellular phase augments local host defense through the entrance of neutrophils and eosinophils that terminate the humoral phase. The activation of mast cells is considered herein in terms of defined physical stimuli that are characterized by urticaria and angioedema.
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PMID:Urticaria, angioedema, and mediator release in humans in response to physical environmental stimuli. 84 16

The i.p. administration of L-histidine in doses of 500 and 1000 mg/kg, caused prolonged high levels of histidine but did not influence the levels of histamine in the non-mast cell tissues such as the stomach, lungs and liver in the rat. After polymyxin B or 48/80 treatments as well as in anaphylaxis, the levels of histamine in the lungs and liver were greatly reduced but histidine administration failed to alter noticeably the concentrations of histamine in these organs. Similarly, the low contents of histamine in the stomach of 48/50-treated or polymyxin B-treated rats remained unchanged in the presence of excess histidine. Histidine loadings however produced a marked increase in histidine decarboxylase activity of the glandular stomach and a simultaneous elevation in the serum histamine concentrations. Results suggest that the increased level of serum histamine is the consequence of the increased activity of histidine decarboxylase in the tissues and a rapid elimination of the newly formed histamine into the blood. This led us to consider that the flux rather than the formation of histamine might be regulatory for the actual concentration of the non-mast cell histamine, especially in stomach tissue.
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PMID:Non-mast cell histamine levels in rat tissues after histidine loading. 85 8

Significant alterations in the circulatory properties of platelets have been documented during IgE-induced systemic anaphylactic shock in the rabbit. Within 30 to 60 sec after i.v. antigen challenge, platelet aggregation occurs in both the venous and arterial circulations. The platelet aggregates then sequester in small blood vessels of various organs, particularly in the lung. The organ sequestration results in the development of a profound thrombocytopenia within 3 to 5 min after antigen challenge. Fifteen min later deaggregation of platelets occurs and the platelets return to the peripheral circulation within normal, prechallenge levels by 60 min. Additional experiments demonstrated that platelet depletion before antigen challenge abrogates the lethal effects and significantly reduces the pathophysiologic manifestations of IgE-induced systemic anaphylaxis. We conclude that the IgE-induced platelet alterations, probably induced by the intravascular release of basophil and perhaps mast cell-derived platelet-activating factor (PAF), play a major role in the pathogenesis of systemic anaphylaxis in the rabbit.
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PMID:Intravascular aggregation and pulmonary sequestration of platelets during IgE-induced systemic anaphylaxis in the rabbit: abrogation of lethal anaphylactic shock by platelet depletion. 91 95

E-type PGs, injected in rat skin at a low dose concentration (1-5 ng ml-) proved not to release vasoactive amines from local mast cell, enhance increase in vascular permeability evoked by hypersensitivity endogenous inflammatory reactions (passive cutaneous anaphylaxis and reversed passive Arthus) or by intradermal injection of histamine and bradykinin. The possible role of PGE1 and PGE2 as modulators of the inflammatory response is discussed.
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PMID:Prostaglandins as modulators of the inflammatory response in the rat. 102 39

A single dose of the yeast-like fungus Candida albicans (CA), mixed with Complete Freund's Adjuvant (CFA), and inoculated into guinea-pig foot-pads, provoked the productions of homologous mast cell sensitizing antibodies (MCSAb) present in the psiI-globulin fraction only, and of agglutinins localized in the same fraction. Heterologous MCSAb and skin-sensitizing antibodies detectable by passive cutaneous anaphylaxis (PCA) were constantly absent. These facts are in contradiction to results of previous experiments performed with other antigens; which after similar inoculation elicited production of heterologous MCSAb attaching themselves on rat mast cells (MC) and present in the psi2 fast moving globulin, homologous MCSAb localized in the psiI-globulin and in the psi2 fast moving globulin, and PCA antibodies. The immunogenicity of CA is discussed.
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PMID:Mast cell sensitizing antibody (MCSAb) response in experimental candidiasis: chromatographic studies. 109 54

The relationship between mast cell degranulation, anaphylaxis, and the production of homocytotropic antibodies was examined in ICR mice after trichinella infection. It was found that the active cutaneous response to trichinella antigen had a rapid onset (within 2 weeks) and the sensitivity increased over a 9-week period after infection. Two types of mast cell degranulation were observed: (i) moderate, with few extracellular, deep-blue-staining granules (May-Grunwald-Giemsa), and (ii) "explosive," with many extracellular reddish-staining, swollen granules, indicating an apparent breakdown of cell membrane. The moderate type was observed primarily during the first 4 weeks after infection, whereas the explosive type predominated during 5 to 8 weeks. Homocytotropic antibody of the immunoglubulin G(1) type appears responsible for moderate type degranulation, and mouse immunoglobulin E appears responsible for the explosive degranulation. No correlation was evident between the active cutaneous anaphylactic response and either type of degranulation or between active cutaneous anaphylaxis and circulating levels of homocytotropic antibody. A proposed role of immunoglobulin G(1) and mouse immunoglobulin E in immunity is discussed.
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PMID:Differential effects of homocytotropic antibodies on the mast cell and anaphylactic responses in actively and passively sensitized mice. 114 Aug 49

In an active cutaneous anaphylaxis induced by DNP-ascaris extract in guinea-pig, tissue eosinophilia manifested two phases; the early and mild phase became maximal in about 6 h, while the delayed and intense phase in 18-24 h. Skin extracts from the lesions exhibited chemotactic activities for eosinophils, respectively comparable to the intensity of tissue eosinophilia in each phase; and two different chemotactic factors for eosinophils of skin extracts were separated by gel filtration on Sephadex G-100. The mediation of the early phase seemed to be associated with a thermostable factor with amolefular weight of less than 1400; this factor seemed to be related to mast cell degranulation. The mediation of the delayed phase appeared to be associated with a thermolabile factor with a molecular weight of about 70,000, probably independent of mast cell degranulation; the factor was considered to be more significant than the thermostable factor, because the delayed tissue eosinophilia was more intense than the early tissue eosinophilia.
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PMID:The mediation of tissue eosinophilia in hypersensitivity reaction. I. Isolation of two different chemotactic factors from DNP-Ascaris extract-induced skin lesion in guinea-pig. 126 51

An attempt of classical conditioning of anaphylaxis by odor was carried out, using actively sensitized guinea pigs with an inhalation of ovalbumin (OA). One month after sensitization, animals were divided into the conditioned group; group C, and the unconditioned group; group U, consisted of 6 animals, respectively. Dimethylsulfied (DMS: sulfur odor), was inhaled in group C as a conditioned stimulus with OA which is an unconditioned stimulus, while only OA was inhaled in group U. Four days after these procedures, saline was inhaled in group C and DMS was solely inhaled in group U in order to equalize the total inhaled dose of OA and DMS in both groups. These sessions were repeated once a week for seven weeks. After final sessions, all animals were inhaled DMS, saline and OA separately, and blood samples were drawn after each inhalation to measure plasma histamine levels. After an inhalation of DMS only, plasma histamine levels of group C and U were 47.5 +/- 9.7 and 25.7 +/- 1.2 ng/ml, respectively. In group C, plasma histamine levels were 32.9 +/- 4.7 at the inhalation of saline and 59.0 +/- 9.2 ng/ml at OA inhalation. Plasma histamine level after an inhalation of DMS only was significantly higher in group C than that in group U (p < 0.05). These results suggest that the conditional stimulus (DMS inhalation) may induce histamine release in the absence of any antigenic stimulus and support the evidence for mast cell-neuron interaction.
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PMID:[Classical conditioning of anaphylaxis in sensitized guinea pigs]. 128 10

Human mast cells were obtained from adenoids and mesentery by enzymatic dispersion of the tissues with the enzyme collagenase. The digestion of the tissues resulted in a cell suspension which contained 1-2% mast cells. 37.3% (adenoids) and 33.4% (mesentery) of total histamine initially present in the tissues was recovered in the dispersed cell suspensions. More than 90% of the cells were viable. The adenoidal mast cells could be sensitized passively in vitro with homologous reaginic serum and released histamine after challenge with specific antigen. Both populations of mast cells were sensitive to the action of anti-human IgE; the reversed anaphylaxis with anti-IgE was higher in mesenteric mast cells. Both examined mast cell populations were sensitive to the challenge with polymyxin B, concanavalin A and ionophore A23187, however, histamine release was only up to 10% and 20% for adenoidal and mesenteric cells, respectively. Only mesenteric mast cells responded to the action of compound 48/80. Histamine release, induced by polymyxin B, was rapid (maximal release within 5 min), maximal in the presence of 3 mM extracellular calcium ions (but also occurred in the absence of the cation).
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PMID:Histamine secretion from human mesenteric and adenoidal mast cells. 128 67

Comparative oligosaccharide analysis by HPLC revealed structural differences in the carbohydrate chains of human IgG4 paraproteins, varying in ability to induce the rhesus monkey's passive skin anaphylaxis. An atypical IgG4 paraprotein, which is inactive in this reaction and also does not bind the IgG4-subclass specific monoclonal antibody IH2, has a much higher proportion of the carbohydrate chains lacking terminal galactose residues than two typical IgG4 paraproteins. This structural feature may be one of the reasons for the atypical IgG4 not to bind by the mast cell Fc gamma receptor.
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PMID:[The structure of carbohydrate chains of human IgG4-paraproteins differing in the ability to bind cell receptors]. 132 72


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