Effect of bilateral adrenalectomy and parenteral betamethasone on gastric mucosal mast cell population in albino rats

Summary The histamine-laden mast cells gastric mucosa in albino rats are shown to degranulate on administration of Betamethasone, but they increase in number in adrenalectomized rats. It is concluded that Betamethasone, and also adrenal glucocorticoids incrase gastric secretion by liberating histamine from mast cells and histamine in turn acts on the gastric glands.     

Effect of pylorus ligation on gastric mucosal mast cell population in normal and adrenalectomised albino rats

Summary Pylorus ligation in normal albino rats acts like a stressor leading to degranulation of mast cells in gastric mucosa, thereby decreasing their number. This decrease is less pronounced when pylorus ligation is done in adrenalectomized rats. This implies that action of a stressor on gastric function involves the adrenal steroids which liberate the powerful gastric stimulant histamine from gastric mucosal mast cells.     

Effect of pylorus ligation on gastric mucosal mast cell population in normal and adrenalectomised albino rats.

Pylorus ligation in normal albino rats acts like a stressor leading to degranulation of mast cells in gastric mucosa, thereby decreasing their number. This decrease is less pronounced when pylorus ligation is done in adrenalectomized rats. This implies that action of a stressor on gastric function involves the adrenal steroids which liberate the powerful gastric stimulant histamine from gastric mucosal mast cells.     

Activation-induced cellular accumulation of histamine in immature but not mature murine mast cells

Mast cell activation involves the rapid release of inflammatory mediators, including histamine, from intracellular granules. The cells are capable of regranulation and multiple rounds of activation. The goal of this study was to determine if there are changes in the content of pre-formed mast cell mediators after a round of activation. After 24 h, the histamine content of bone marrow-derived mast cells (BMMC), but not that of peritoneal mast cells, exceeded the amount in resting cells. Accumulation of histamine in BMMC peaked at 72 h of activation, and returned toward preactivation levels by 96 h. The increase in histamine content was accompanied by an increase in the gene expression of histidine decarboxylase. No increases in beta hexosaminidase or murine mast cell protease-6 were observed. These findings indicate that BMMC respond to activation by increasing total cell-associated histamine content. This increase may be important to the response of these cells upon subsequent exposure to antigens.     

Smallest zinc quantities affect the histamine release from peritoneal mast cells of the rat

Seven individual 0.025-mg doses of zinc administered as lactose tablets on consecutive days, significantly increase histamine release from peritoneal mast cells of the rat. Seven individual doses of 0.25 microgram caused a somewhat smaller, though still very pronounced increase in the release in comparison with zero control.     

Gastrin: obligatory intermediate in the postprandial mobilization of gastric histamine in the rat.

In unoperated fasted rats, feeding raised the serum gastrin concentration, reduced the gastric mucosal histamine content and activated the gastric histidine decarboxylase. The reduction of gastric histamine and activation of histidine decarboxylase was induced also by the injection of pentagastrin. In antrectomized rats, feeding failed to produce these effects. Injection of pentagastrin, however, still lowered gastric histamine and activated gastric histidine decarboxylase. Thus, antral gastrin seems to be an obligatory mediator of the postprandial activation of histidine decarboxylase and mobilization of histamine.     

Role of calcium in the histamine release induced by D-galactosamine from rat mast cells

Rat peritoneal mast cells were isolated and purified by differential centrifugation in Ficoll. Cells pooled from three to four rats were suspended at approximately 10(6) cells/ml in a buffered salt solution and incubated for 1 h at 37 degrees C in 300 microliter volumes in the absence or presence (9 X 10(-4) M) of calcium chloride. Addition of D-galactosamine hydrochloride (DGM; 2.8 X 10(-4)M) caused (in addition to basal release) a mean +/- SEM percent histamine release of 15.7 +/- 5.2 in the presence of Ca++ and 19 +/- 4.9 in the absence of Ca++ (p greater than 0.05). It is suggested that D-galactosamine does not require extracellular Ca++ for the release of histamine from the rat mast cell.     

Allergic reactions, cyclic AMP and histamine release.

Both isobutylmethylxanthine and theophylline increased the level cyclic AMP in the mast cell. Theophylline reduced the allergic histamine release, whereas isobutylmethylxynthine caused a pronounced potentiation of the histamine release. This indicates that the hypothesis of an inverse relationship between the level of cyclic AMP in mast cells and histamine release is too simple.     

Gastrin: Obligatory intermediate in the postprandial mobilization of gastric histamine in the rat

Summary In unoperated fasted rats, feeding raised the serum gastrin concentration, reduced the gastric mucosal histamine content and activated the gastric histidine decarboxylase. The reduction of gastric histamine and activation of histidine decarboxylase was induced also by the injection of pentagastrin. In antrectomized rats, feeding failed to produce these effects. Injection of pentagastrin, however, still lowered gastric histamine and activated gastric histidine decarboxylase. Thus, antral gastrin seems to be an obligatory mediator of the postprandial activation of histidine decarboxylase and mobilization of histamine.Acknowledgments. Grant support from the Swedish and Danish Medical Research Councils (14P-4822, 04X-1007, 17X-4144 and 512-2540).     

Histamine binding to H2 receptors stimulates phospholipid methylation in mast cells

Summary Rat peritoneal mast cells incubated in vitro in the presence of L-[methyl-³H] methionine and exposed to histamine undergo a rapid but transient increase in phospholipid methylation. By using specific H₁- and H₂-receptor antagonists, and histamine analogues differing in their H₂-receptor agonist potency, it has been demonstrated that this metabolic event is dependent on histamine binding to H₂-receptors.We are grateful to Smith Kline and French Laboratories for the generous gift of histamine analogues.     

Mechanism of inhibition of IgE-dependent histamine release from rat mast cells by xestobergsterol A from the Okinawan marine spongeXestospongia bergquistia

Histamine release from rat peritoneal mast cells induced by anti-IgE was essentially complete within 4–5 min. Xestobergsterol A and B, which are constituents of the Okinawan marine spongeXestospongia bergquistia Fromont, dose-dependently inhibited anti-IgE-induced histamine release from rat mast cells. The IC₅₀ values of xestobergsterol A and B for histamine release in mast cells activated by anti-IgE were 0.07 and 0.11 M, respectively. Anti-IgE stimulated PI-PLC activity in a mast cell membrane preparation. Xestobergsterol A dose-dependently inhibited the generation of IP3 and membrane-bound PI-PLC activity. Moreover, xestobergsterol A inhibited Ca²⁺-mobilization from intracellular Ca²⁺-stores as well as histamine release in mast cells activated by anti-IgE. On the other hand, xestobergsterol B did not inhibit the membrane-bound and cytosolic PI-PLC activity, IP3 generation or the initial rise in [Ca²⁺]_i in mast cells activated by anti-IgE. These results suggest that the mechanism of inhibition by xestobergsterol A of the initial rise in [Ca²⁺]_i, of the generation of IP3, and of histamine release induced by anti-IgE, was through the inhibition of PI-PLC activity.     

Allergic reactions,cyclic AMP and histamine release

Summary Both isobutylmethylxantine and theophylline increased the level of cyclic AMP in the mast cell. Theophylline reduced the allergic histamine release, whereas isobutylmethylxynthine caused a pronounced potentiation of the histamine release. This indicates that the hypothesis of an inverse relationship between the level of cyclic AMP in mast cells and histamine release is too simple.This work was supported by grants from the Danish Medical Research Council (Grant No. 512-5270) and from Lundbeckfonden.     

Biological implications of preformed mast cell mediators

Mast cells store an impressive array of preformed compounds (mediators) in their secretory granules. When mast cells degranulate, these are released and have a profound impact on any condition in which mast cell degranulation occurs. The preformed mast cell mediators include well-known substances such as histamine, proteoglycans, proteases, and preformed cytokines, as well as several recently identified compounds. Mast cells have recently been implicated in a large number of novel pathological settings in addition to their well-established contribution to allergic reactions, and there is consequently a large current interest in the molecular mechanisms by which mast cells act in the context of a given condition. In many cases, preformed mast cell mediators have been shown to account for functions ascribed to mast cells, and these compounds are hence emerging as major players in numerous pathologies. In this review we summarize the current knowledge of preformed mast cell mediators.     

Effect of daily parenteral injection of betamethasone on histamine concentration of gastric tissue in albino rats

Gastric tissue histamine concentration was determined in albino rats following daily parenteral injection of betamethasone over a period of 12 days. The result shows a highly significant fall in gastric tissue histamine concentration in comparison with that in saline-treated albino rats over a similar period.     

Immuno-electron microscopic localization of fibronectin on rat mast cells

Summary Rabbit anti-rat plasma fibronectin (pFN) causes histamine release from rat mast cells in the presence of complement. Fibronectin (FN) on rat mast cells, as shown by immuno-electron microscopy, is principally localized on cell folds, so they may play a role of attachment in the matrix of connective tissue.Acknowledgment. This work is supported by grants (No. 56770014 and No. 544018) from the Ministry of Education, Science and Culture of Japan.     

A comparative study of the gastric ulcerogenic effects of stress and reserpine in rats with decreased stomach wall mast cell populations

Summary Stress-induced gastric glandular ulcers in rats appeared less severe than those evoked by reserpine, although glandular mucosal mast cell counts were equally decreased. Prior depletion of the glandular mucosal mast cell population confirmed the hypothesis that an additional mechanism contributes to reserpine ulceration.     

Smallest zinc quantities affect the histamine release from peritoneal mast cells of the rat

Summary Seven individual 0.025-mg doses of zinc administered as lactose tablets on consecutive days, significantly increase histamine release from peritoneal mast cells of the rat. Seven individual doses of 0.25 g cause a somewhat smaller, though still very pronounced increase in the release in comparison with zero control.Acknowledgments. We thank Ms T. L. Pham and Ms K. Löppen for their technical assistance.     

Effect of daily parenteral injection of betamethasone on histamine concentration of gastric tissue in albino rats

Summary Gastric tissue histamine concentration was determined in albino rats following daily parenteral injection of betamethasone over a period of 12 days. The result shows a highly significant fall in gastric tissue histamine concentration in comparison with that in saline-treated albino rats over a similar period.This investigation was carried out as a part of a project supported by a research grant from Medical Research Centre, Bombay Hospital Trust, Bombay, India.     

Mast cells in the skin of normal,hairless and athymic mice

Summary The skin of congenitally athymicnu/nu mice is rich in mast cells which stain metachromatically, contain histamine and 5-hydroxytryptamine, and participate in the PCA reaction. Mast cells of athymic mice have thus the attributes of normal mast cells.This work was supported by grants from the Swiss National Science Foundation (No. 3.516.71 and 3.234.74) and the Fritz Hoffmann-La-Roche-Stiftung.The skilful technical assistance of MissR. Keist is gratefully acknowledged.     

Role of calcium in the histamine release induced by D-galactosamine from rat mast cells

Summary Rat peritoneal mast cells were isolated and purified by differential centrifugation in Ficoll. Cells pooled from three to four rats were suspended at approximately 10⁶ cells/ml in a buffered salt solution and incubated for 1 h at 37°C in 300 l volumes in the absence or presence (9×10^–4 M) of calcium chloride. Addition of D-galactosamine hydrochloride (DGM; 2.8×10^–4 M) caused (in addition to basal release) a mean ±SEM percent histamine release of 15.7±5.2 in the presence of Ca⁺⁺ and 19±4.9 in the absence of Ca⁺⁺ (p>0.05). It is suggested that D-galactosamine does not require extracellular Ca⁺⁺ for the release of histamine from the rat mast cell.A preliminary analysis of these results was presented at the International Symposium on calcium entry blockers and tissue protection, Rome, 15–16 March 1984.