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

Suspensions of rat mast cells were used to study the histamine-releasing actions of anaphylatoxins C3A and C5a in vitro. The peptides, derived from human or porcine complement proteins C3 and C5, were less potent than 48/80 but more potent than bradykinin in stimulating release of histamine from mast cells. The pattern of release resembled that of the anaphylactic release action, e.g. release was limited to less than 30 per cent of the cell histamine, the reaction was calcium-dependent and was potentiated by phosphatidyl serine. When C3a and C5a were added together to mast cell suspensions, the amount of histamine released was additive. Similarly, release by either peptide combined with bradykinin was additive. Histamine-releasing activity (as well as smooth muscle-stimulating activity) was abolished when the peptides were treated with pancreatic carboxy-peptidase B. Active or inactive peptides were bound by mast cells and addition of active C3a in combination with the inactive, des-arginine derivative, C3ai, resulted in partial inhibition of histamine release.
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PMID:Release of histamine from rat mast cells by the complement peptides C3a and C5a. 4 5

We have used ferritin-conjugated divalent and monovalent anti-Ig antibodies to study simultaneously, histamine secretion and the ultrastructural distribution and redistribution of Ig receptors on rat peritoneal mast cells. We conclude that (a) divalent anti-Ig is required for both receptor redistribution and for calcium-dependent degranulation and histamine release, (b) divalent anti-Ig induces patching and pinocytosis but not capping of Ig molecules, (c) neither capping nor pinocytosis are required for triggering and if clustering is necessary, then less than 10 Ig molecules are required per cluster, and (d) degranulation (and histamine release) is not an all or none response of the mast cell.
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PMID:Anti-immunoglobulin-induced histamine secretion by rat peritoneal mast cells studied by immunoferritin electron microscopy. 4 87

Rats were maintained on a magnesium-deficient diet for 1 to 5 weeks to study the mast cell (MC) populations in their duodenum and kidney. A marked increase of intestinal subepithelial mast cells was observed in these animals as compared with normal controls. The cells in both groups showed an identical reaction for mucopolysaccharides but the 5-hydroxytryptamine content tended to be higher in the cells of magnesium-deficient animals. Proliferation of MC was also observed in the renal cortex of the magnesium-deficient rats. This finding is significant because MC are known to be virtually absent from normal kidneys. Magnesium deprivation resulted in numerous MC not only in the intertubular spaces but also within the glomeruli. Possible correlations between these and other pertinent observations are discussed with regard to certain renal diseases. The discussion is extended to the possible mechanism through which magnesium could influence secretory processes in MC.
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PMID:Mast cell increase in the duodenum and kidney of magnesium-deficient rats. 4 55

Cobra venom, alone and in combination, on mast cell degranulation, histamine release and formation of prostaglandin-like activity (SRS-C) was studied in perfused guinea-pig lungs and in mast cell-containing rat peritoneal cell suspensions. For comparison, the effect of equivalent doses of whole cobra venom was investigated. 1. Cobra venom caused mast cell degranulation, histamine release and SRS-C formation in both systems. For comparable effects much higher doses had to be used in guine-pig lungs than in rat peritoneal cell suspensions. 2. Phase A showed little degranulation of mast cells in both systems, a limited histamine release in rat peritoneal cell suspensions and none in perfused guinea-pig lungs. It caused a considerable SRS-C formation in both, lung tissue and peritoneal cell suspensions. 3. DLF caused histamine release, SRS-C formation and mast cell degranulation in both systems; in rat peritoneal cell suspensions it acted almost as strong as equivalent doses of cobra venom, in guinea pig lungs it was much less active. 4. In rat peritoneal cell suspensions the effects of DLF and phase A in combination did not exceed the sum of their single effects. In guinea-pig lungs these two substances interacted in a potentiating synergism. It is concluded that DLF is the main cytotoxic principle of cobra venom, whereas ph-ase A alone is not cytotoxic. The difference in the synergism of DLF and ph-ase A between rat peritoneal cells and guinea-pig lungs may be due to two different actions of DLF and species differences as regards sensitivity against these actions.
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PMID:Histamine release, formation of prostaglandin-like activity (SRS-C) and mast cell degranulation by the direct lytic factor (DLF) and phospholipase A of cobra venom. 4 54

A practical, simple synthesis of the obsolete mordant dye, phenocyanin, was devised, proceding from gallocyanin and resorcinol with acid and heat. The dye gave promise of good performance in metachrome iron mixtures, but because of excessive precipitation, the practice of afterchroming was taken from textile dyeing usage, and proved very successful. Of a number of metallic salts tried, Fe II proved to be the best, then Cu II and Fe III. The stain acts as a cationic dye on nucleic acids and other acidic tissue components: acid mucins, cartilage, mast cells, corpora amylacea, etc. The afterchroming process renders the stain much more resistant to various extraction agents and even moderately resistant to acid alcohol. Color values are quite comparable to those obtained with hematoxylin-eosin when an eosin counterstain is used. Nuclei basophilic cytoplasm, Nissl granules, and bacteria color dark blue; cartilage, mast cells, and some acid mucins, deep violet. Staining with the 1% solution was essentially unaltered from neutrality down to 1.2 N HCl, pH 0.68, and dilution of the dye to 0.05% in 1% conc. HCl (pH 1.2) still gave excellent nuclear, RNA, and mast-cell staining. At 0.02% and pH 1.2, nuclear staining was distinctly weakened; mast cell granules were still dark violet.
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PMID:Hematoxylin substitutes. A study of phenocyanin TC and the use of afterchrome mordanting in histology. 5 6

1. The effects of intraperitoneal injections of actinomycin D on the temporal characteristics of the accumulation of the inflammatory exudate and cells into the peritoneal and pleural cavities were studied in male Sprague Dawley rats. 2. A measurable quantity of the exudate appeared in both cavities within 24 h and reached maxima in the peritoneal and pleural cavities on the fourth and third days, respectively. Thereafter, the accumulated volume of liquid decreased progressively in the peritoneal cavity but stayed more or less at about the same level in the pleural cavity until the sixth day. 3. The pooled peritoneal and pleural exudates contained neutrophils, macrophages, mast cell and eosinophils. The leucocyte infiltration occurred in two phases, the maximum cell numbers being found on the third and fifth days. A precipitous fall in the number of leucocytes occurred on the fourth day. Neutrophils and macrophages accounted for 85-95% of the total number of leucocytes. 4. The supernatant of the inflammatory exudate after centrifugation at 3,000 g contained histamine and the soluble lysosomal enzyme proteins, acid phosphatase and beta-glucuronidase until the sixth day following the initial dose of actinomycin D. 5. It is suggested that the release of lysosomal enzymes in the exudate, subsequent to leucocyte mobilization and the release of histamine from the mast cells, are probably involved in the genesis of inflammatory conditions induced by actinomycin D.
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PMID:Mobilization of leucocytes and subsequent release of histamine and lysosomal enzymes into the peritoneal and pleural cavities of rats by actinomycin D (dactinomycin). 5 Jan 58

Lectins from Ricinus communis and Glycine max, as well as wheat germ agglutinin and concanavalin A, caused a dose-dependent release of histamine from mast cells present in the mixed peritoneal cells from the rat. In addition, histamine release in an IgE-mediated and a compound 48/80-mediated reaction was inhibited in cells which had been pretreated with these lectins. With concanavalin A and the R. communis lectin both effect were prevented by the addition of the appropriate monosaccharides to the incubations. However, the lectin-induced histamine release and the lectin-induced inhibition of subsequent IgE-mediated histamine release could be dissociated: thus L-rhamnose, a hexose not ordinarily found on mammalian cell membranes, a specifically inhibited histamine release which was caused by the lectin from R. communis without affecting the inhibition of IgE-mediated histamine release. Conversely, D-fucose, which also is not a constituent of cell membrane glycolipids or glycoproteins prevented the inhibition of IgE-mediated histamine release by this lectin without affecting the lectin-induced histamine release. Furthermore, the nominally galactose-specific lectins from Sophora japonica and Ulex europeus inhibited IgE-mediated histamine release while causing little if any histamine release themselves. High concentrations of the lectin from Lotus tetragonolobus failed to cause histamine release or to affect the IgE-mediated histamine release reaction. Based on the known structural specificity of these lectins and the amounts of the lectins which were required to demonstrate an effect, it was concluded that D-galactose, alpha-linked, intrachain D-glucose (or mannose), and N-acetylglucosamine residues but probably not N-acetyl-galactosamine or L-fucose residues in the glycolipids or glycoproteins of the mast cell membrane can play a role in the initiation of histamine release and in the desensitization of the cells to subsequent histamine release-inducing stimuli.
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PMID:Inhibition of IgE and compound 48/80-induced histamine release by lectins. 5 Oct 3

The binding of human myeloma IgE immunoglobulin on rat mast cells was studied by three independent techniques. A mixed agglutination reaction with anti-IgE-coated Sephadex granules demonstrated that only human IgE-coated rat mast cells were clearly agglutinated. This binding is strong (50% agglutination) in 3 min and progresses for 30 min (95% agglutination). Autoradiographic studies with 125I-labelled human serum proteins demonstrated the selective formation of grains on mast cells incubated with labelled IgE. Upon action of anti-IgE antiserum on IgE-coated rat mast cells, the mast cells released up to 47.5% of their total histamine content in a fluorometric histamine assay. A relationship was established between sensitizing doses of human IgE and histamine release. These results bring evidence for a binding of human IgE on rat mast cells and imply the existence of receptors for this immunoglobulin on mast cell membrane.
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PMID:Binding of human IgE immunoglobulin to rat mast cells. A study by means of three independent techniques. 5 Oct 10

The concentration of IgE in the serum of Sprague-Dawley rats increased after infection with Nippostrongylus brasiliensis (NB). The IgE concentration in normal rats was less than 1 mug/ml. After re-infection with NB, the concentration increased in 100 to 300 mug/ml. Mast cells were purified from peritoneal cells of both normal and NB-infected animals. Purified mast cells from the infected animals released histamine upon exposure to NB antigen. The antibody specific for IgE released histamine from purified mast cells of both normal and infected animals. Dose-reponse curves of histamine release suggested that mast cells from NB-infected animals bear more IgE molecules than normal mast cells. Binding of 125I-labeled rat E myeloma protein with normal mast cells was demonstrated by autoradiography. Under the same experimental conditions, mast cells of infected animals were not labeled with 125I-IgE. Mast cells from both normal and infected animals failed to combine 125I-labeled IgG. The number of IgE molecules bound per mast cell was determined by incubating 125I-labeled IgE with purified mast cells. When mast cells were incubated incubated in 0.6 to 2 mug/ml of IgE, the number of IgE molecules combined with the mast cells from infected animals was about 10% of that bound with normal mast cells. The results indicated that a large proportion of IgE receptors on mast cells of infected animals was occupied by their own IgE. No significant difference was observed between normal mast cells and those of infected animals with respect to histamine content and intracellular levels of cyclic nucleotides.
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PMID:Immunologic properties of mast cells from rats infected with Nippostrongylus brasiliensis. 5 73

Acid mucopolysaccharides in mast cell granules were histochemically studied in the lesion of urticaria pigmentosa and in the dermis of normal human skin. Alcian blue and azure A were used to stain mucopolysaccharides. Bromphenol blue was employed for detection of basic proteins. In a further attempt to identify various polyanions, staining was carried out with alcian blue containing various concentrations of electrolytes. Methylation, saponification, and digestion with streptomyces or testicular hyaluronidase, chondroitinase ABC, sialidase, or desoxyribonuclease were also employed. The results obtained are most likely to suggest the presence of hyaluronic acid in mast cell granules.
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PMID:Histochemical demonstration of hyaluronic acid in human dermal mast cells. 5 4


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