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

Acid secretory effect of pentagastrin and compound 48/80 was studied in the isolated whole stomach of the mouse. Acid secretory response to compound 48/80 was inhibited by cimetidine, indicating histamine involvement in this reaction. Acid secretion stimulated by pentagastrin was not diminished after pre-treatment with compound 48/80 suggesting that gastrin releases non-mast cell histamine. Secretory response to pentagastrin was reduced in Ca++-free serosal media but not to histamine and compound 48/80. A possible pathway of gastrin will be discussed.
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PMID:Does gastrin (pentagastrin) act directly on the parietal cell in the isolated whole stomach of the mouse? 12 66

After a review on the historical development of morphological investigations of entero-endocrine cells, dating back to 1870, a detailed synoptical review of the current stage of findings in this field is given. At the present time nine different endocrine cell types can be distinguished in the epithelium of the gastrointestinal tract. Criteria for this differentiation are properties concerning specific staining methods, aldehyde-induced fluorescence, immunohistochemistry, and ultrastructure. From present results it is obvious that distinct cell types are responsible for the synthesis of defined polypeptide hormones (e.g. gastrin, secretin, enterogastrone). The metabolism of amines, in relation to the endocrine cells of the gastrointestinal tract is of particular interest here. Points investigated include the uniqueness of endocrine cells, with regard to the metabolism of biogenic amines ("APUD-cells") and the possibility of serotonin synthesis by a definite cell type, i.e. by the EC-cell ("enterochromaffin" cell). In our experimental animal, male Wistarrats, seven different entero-endocrine cell types can be discerned by ultrastructural means: EC-, ECL-, G-, AL-, EG-, D- and D1-cells. The I-cell (found in other species) can hardly be distinguished from the AL-cell by ultrastructural means and the S-cells, as found in other species, are not to be found at all. Only some of the cited cell types can be seen by fluorescence microscopy. After formaldehyde-treatment of the tissue, the "enterochromaffin" cell shows a yellow, serotonin-specific fluorescence. This cell corresponds in shape, number and distribution to the ultrastructurally defined EC-cell. EC-cells are found predominantly in the pyloric region and the duodenum and less frequently in the middle- and hindgut and the cardiac region; seldomly EC-cells are encountered in the oxyntic gland area of the stomach. In the rat gastro-intestinal tract, number and fluorescent intensity of EC-cells does not always correspond with the serotonin content of a certain region--sometimes the level of serotonin is largely determined by the mast cells, which in the rat also contain serotonin. For example, the high serotonin content of the oxyntic gland area, which contains very few EC-cells, has to be contributed nearly exclusively to mast cell serotonin. Mast cells can be domonstrated by fluorescence microscopy, due to their histamine content, after treatment of the tissue with o-phthalaldehyde (OPD). It seems likely that the histamine content, especially that of the so-called "atypical mast cells" of the mucosa, is inversely related to their respective serotonin content. --In addition to mast cells, OPD-treatment leads to a fluorescence in some of the entero-endocrine cells of the gastrointestinal epithelium. In the gastric epithelium these fluorescing cells should be regarded as histamine-containing ECL-cells and glucagon-containing AL-cells while in the colonic epithelium they are considered to be glucagon-containing AL-cells...
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PMID:[The endocrine cells of the gastrointestinal epithelium and the metabolism of biogenic amines in the gastrointestinal tract (author's transl)]. 13 9

The regulation of histamine release from oxyntic mucosa is complex because of two potential sources of histamine: mast cells and enterochromaffin-like (ECL) cells. A gastrin-responsive histamine pool was identified in the rat oxyntic mucosa two decades ago, but these ECL cells from the rat have not yet been isolated or characterized in vitro. In vivo studies in canine and human mucosa have been more difficult because of the high content of histamine in mast cells. Using enzyme-dispersed canine oxyntic mucosal cells, we have studied regulation of histamine release from a mast cell-depleted fraction prepared by sequential elutriation and density gradient. Histamine-like immunoreactivity was demonstrated, using peroxidase-anti-peroxidase immunohistochemistry. After short-term culture, histamine was released in response to gastrin, cholecystokinin, carbachol, and forskolin. Somatostatin potently and effectively inhibited the response to gastrin. The cultures used for these studies also contained somatostatin cells, and, furthermore, the response to gastrin was enhanced by incubation with monoclonal antibodies to somatostatin. The latter findings suggested that somatostatin was acting in these cultures by a paracrine route. This pattern contrasts with that obtained in previous studies of canine oxyntic mucosal mast cells.
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PMID:Regulation of histamine release from oxyntic mucosa. 128 99

Using enzyme-dispersed canine oxyntic mucosal cells, we studied regulation of histamine release from fractions in which mast cells were largely removed by density gradient. Histamine-like immunoreactivity was demonstrated using peroxidase-anti-peroxidase immunohistochemistry. Histamine-containing cells in the small cell elutriator fractions (SCEF) were further separated by albumin step density gradients. Approximately 2.5% of cells in the low density fraction (LDF) contained histamine-like immunoreactivity; this fraction was largely depleted of the more dense mast cells (0.5%). These two fractions were cultured for 48-64 h on a Matrigel substrate. The cell content of histamine and release into the medium were measured by radioenzymatic assay. Gastrin, carbachol, and forskolin increased histamine release from the LDF. The induction of histamine release by gastrin was evident within 5 min and was sustained for at least 60 min. The response to gastrin was dose dependent between concentrations of 10(-11) and 10(-8) M. In contrast, in the mast cell-enriched SCEF, basal release was higher and gastrin was without effect; however, concanavalin A stimulated and epinephrine inhibited histamine release indicating that histamine-release mechanisms were intact in this fraction. Our methods provide a preparation of low density oxyntic mucosal histamine cells that demonstrate gastrin-responsive histamine release; we speculate that enterochromaffin-like cells account for this gastrin response.
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PMID:Gastrin induction of histamine release from primary cultures of canine oxyntic mucosal cells. 138 57

Fasting gastrinemia, fundic argyrophil cell density, mast cell number, basal fundic histamine content and histidine decarboxylase activity were determined in 20 antrectomized patients and 20 control subjects. Fasting gastrinemia and fundic argyrophil cell density were significantly lower in antrectomized patients than in controls, whereas fundic mast cell number, basal histamine content, and histidine decarboxylase activity did not differ significantly between the two groups. In antrectomized patients the basal fundic histamine content appears related to the fundic mast cell number, as a consequence of the reduced effect of gastrin on argyrophil cells.
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PMID:Argyrophil cells, mast cells, and histamine in the fundic mucosa of antrectomized patients. 143 47

Peptides such as parathyroid hormone (PTH), somatostatin, and gastrin have been reported to stimulate mast cell mediator release. Preincubation of rat serosal mast cells with synthetic 1-34 bovine parathyroid hormone (1-34bPTH) significantly enhanced antigen-induced 5-hydroxytryptamine (5-HT) release. Enhancement of 5-HT release by 1-34bPTH was dose dependent between 5 and 2000 nM. In the absence of antigen, mean net 5-HT release was less than 1% when naive or passively sensitized mast cells were incubated with 1000 nM 1-34bPTH for time intervals up to 90 min. These findings indicate that 1-34bPTH, at relatively low concentration, potentiates antigen-induced 5-HT release from mast cells.
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PMID:Potentiation of antigen-induced mast cell activation by 1-34 bovine parathyroid hormone. 202 Jun 69

Dogs with mast cell tumors (MCT) are often affected with paraneoplastic syndromes such as gastrointestinal ulceration. The mechanism of ulceration is believed to be related to hyperhistaminemia. To test this hypothesis, plasma histamine and gastrin concentrations were measured in 17 dogs with MCT. Plasma histamine concentrations in dogs with MCT were significantly higher than those in normal dogs. Conversely, plasma gastrin concentrations in dogs with MCT were significantly lower than gastrin concentrations in normal dogs. Additionally, plasma gastrin concentrations were inversely related to plasma histamine concentrations, which provided indirect evidence for the presence of hyperacidity secondary to hyperhistaminemia (r2 = 57.7). Plasma histamine and plasma gastrin concentrations were not related to clinical stage of disease, tumor histologic grade, or tumor size. Median survival time was 245 days, with a range of 90 to 1315 days. Because the degree of hyperhistaminemia could not be predicted in this study from the clinical stage, histologic grade, or tumor size, these data suggest that hyperhistaminemia may occur in any dog with MCT.
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PMID:Plasma histamine and gastrin concentrations in 17 dogs with mast cell tumors. 212 27

Recent research has disclosed that neurotransmitters and neuropeptides released within the autonomic nervous system exert homeostatic control of nasal secretion. Although cholinergic and adrenergic influences have long been thought to be the predominant mechanisms, the nonadrenergic, noncholinergic responses may have more suitable, longer-lasting effects. Peptides from sensory nerves, such as calcitonin gene related peptide, substance P, and neurokinin A, may participate in axon response-mediated vasodilation and plasma extravasation. Substance P and gastrin releasing peptide may induce glandular secretion. Defensive responses to local mucosal injury may be amplified by axon response, which initiates these vascular and glandular reactions. Cholinergic effects are primarily responsible for mediating parasympathetic reflexes, but vasoactive intestinal peptide may regulate acetylcholine release, augment glandular secretory responses, and have a vasodilatory effect. In the sympathetic nervous system, neuropeptide Y probably functions as a long-acting vasoconstrictor. Integration of sympathetic and parasympathetic influence may regulate the normal nasal cycle, and sensory and parasympathetic defensive reflexes may respond to epithelial and mast cell stimulation. It is possible, then, that the pathophysiology of vasomotor rhinitis involves an exaggeration of these neural influences.
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PMID:Neuropeptides and nasal secretion. 222 24

Between 1971 and 1986 532 proximal gastric vagotomies were carried out at the Pelgulinna Hospital. The five-year recurrence rate was 5.5% (n = 29). We have studied 40 patients with chronic duodenal ulceration, 20 patients who had effective proximal gastric vagotomy, and seven patients who presented with recurrent ulcers after proximal gastric vagotomy. Patients who had positive Hollander tests after vagotomy, and those with disorders of gastric motility, were excluded. In the group with recurrent ulcers the concentration of neutral mucopolysaccharides in the gastric juice was significantly lower than in the other two groups, and it correlated with the amount of material showing a positive reaction to periodic acid Schiff (PAS) in the gastric mucosa. This group also had significantly higher mean serum gastrin concentrations and mast cell degranulation rates in the mucosa of the fundus and the antrum. We conclude that qualitative changes in the production of gastric mucus lead to defective functioning of the mucosal barrier in patients with recurrent ulcers and may be one of the causes of recurrences.
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PMID:Recurrent ulceration after proximal gastric vagotomy. Possible role of mucosal barrier. 226 41

The effect of a high dose of omeprazole on the plasma gastrin response to feeding and gastric mucosal histamine formation and storage in the dog has been studied. Tissue from the oxyntic gland area was obtained by introduction of an endoscope through a gastric fistula, and biopsies were taken before, after 4 weeks of oral administration of omeprazole and 1 month after withdrawal of the drug. Omeprazole administration increased the basal plasma concentration of gastrin and induced a substantial increase in the feeding response. Histidine-decarboxylase activity was significantly increased after 4 weeks of omeprazole administration, whereas no effect was found on histamine content and mucosal mast cell density. One month after drug withdrawal, the enzyme activity had returned to pretreatment levels.
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PMID:Effect of high-dose omeprazole administration on histamine storage and formation in canine gastric mucosa. 365 27


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