The Activation of Mast Cells by the Histamine Liberator 48/80 in Man

1963 ◽  
Vol 22 (6) ◽  
pp. 408-415 ◽  
Author(s):  
Federigo Sicuteri ◽  
Sergio Michelacci ◽  
Giancarlo Franchi
Keyword(s):  
Mast Cells ◽  
Histamine Liberator

scholarly journals CYTOLOGICAL AND PHARMACOLOGICAL OBSERVATIONS ON THE RELEASE OF HISTAMINE BY MAST CELLS

1954 ◽  
Vol 100 (2) ◽  
pp. 217-224 ◽  
Author(s):  
Don W. Fawcett
Keyword(s):  
Mast Cells ◽  
Peritoneal Fluid ◽  
Appreciable Amount ◽  
Fluid Solution ◽  
Tyrode Solution ◽  
Morphological Effect ◽  
Liberation Of Histamine ◽  
To Come ◽  
Histamine Liberator ◽  
Extensive Release

Experimental solutions known to affect mast cells or to cause liberation of histamine from the tissue were introduced into the peritoneal cavity of rats. Samples of the peritoneal fluid were withdrawn at intervals afterward and assayed for histamine and the condition of the mast cells was subsequently ascertained by microscopic examination of stained spreads of the mesenteries. Intraperitoneal injection of distilled water caused osmotic disruption of the mast cells and the appearance of an appreciable amount of histamine in the peritoneal fluid. Injection of Tyrode solution alone was not particularly damaging to the mast cells and little or no histamine was released. Injection of Tyrode solution containing compound 48/80 resulted in extensive release of granules from mast cells and the appearance of large amounts of histamine in the fluid. Solution of 48/80 failed however to cause histamine release when injected into rats whose subserosal mast cells had previously been destroyed. A series of increasing doses of compound 48/80 had a graded morphological effect upon mast cells and resulted in a graded increase in the amount of histamine that appeared in the peritoneal fluid. It is unlikely therefore that this compound acts by simply lysing the plasma membrane. It is concluded that mast cells in the rat are extraordinarily rich in histamine which is liberated under conditions which cause mast cells to release their granules. The histamine set free by the potent histamine liberator, compound 48/80, appears to come principally from the tissue mast cells.

Increase in histidine decarboxylase activity of rat skin following treatment with compound 48/80

1959 ◽  
Vol 196 (2) ◽  
pp. 295-298 ◽  
Author(s):  
Richard W. Schayer ◽  
Zuleika Rothschild ◽  
Piroska Bizony
Keyword(s):  
Mast Cells ◽  
Histidine Decarboxylase ◽  
Probable Mechanism ◽  
Decarboxylase Activity ◽  
Rat Skin ◽  
Duration Of Treatment ◽  
Histological Studies ◽  
Histamine Liberator ◽  
Histidine Decarboxylase Activity ◽  
Intact Rats

Repeated injections of rats with compound 48/80, a histamine liberator, results in a marked increase in histidine decarboxylase activity of the skin. The increase is roughly proportional to the duration of treatment. This eliminates activation of pre-existing histidine decarboxylase as a probable mechanism. The increase can be demonstrated in intact rats; therefore, rat skin histidine decarboxylase is an adaptive enzyme. It seems probable that 48/80 treatment leads to the production of new, resistant mast cells which are particularly active in forming histamine. This speculation is compatible with reports from other laboratories of histological studies on rats given 48/80. Implications of this finding are discussed.

EFFECT OF MAGNESIUM DEFICIENCY ON THE REGENERATION OF MAST CELLS AFTER TREATMENT WITH 48/80 IN RATS

1960 ◽  
Vol 38 (1) ◽  
pp. 585-589 ◽  
Author(s):  
Pierre Bois ◽  
Ernest H. Byrne ◽  
Leonard F. Bélanger
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Guinea Pig ◽  
Cell Population ◽  
Magnesium Deficiency ◽  
Guinea Pig Ileum ◽  
Deficient Diet ◽  
Cell Counts ◽  
Histamine Liberator ◽  
Mast Cell Population

The decrease in subcutaneous mast cell population observed in rats on a magnesium-deficient diet has been confirmed. Pretreatment with histamine liberator compound 48/80 accentuates the decrease in mast cell counts. This condition was apparently the result of defective regeneration. The decrease in the number of subcutaneous mast cells was accompanied by a parallel reduction of histamine as appreciated by the guinea pig ileum assay. The peripheral vasodilation, which is an early sign of magnesium deficiency, did not appear in rats pretreated with 48/80.

EFFECT OF MAGNESIUM DEFICIENCY ON THE REGENERATION OF MAST CELLS AFTER TREATMENT WITH 48/80 IN RATS

1960 ◽  
Vol 38 (6) ◽  
pp. 585-589 ◽  
Author(s):  
Pierre Bois ◽  
Ernest H. Byrne ◽  
Leonard F. Bélanger
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Guinea Pig ◽  
Cell Population ◽  
Magnesium Deficiency ◽  
Guinea Pig Ileum ◽  
Deficient Diet ◽  
Cell Counts ◽  
Histamine Liberator ◽  
Mast Cell Population

The decrease in subcutaneous mast cell population observed in rats on a magnesium-deficient diet has been confirmed. Pretreatment with histamine liberator compound 48/80 accentuates the decrease in mast cell counts. This condition was apparently the result of defective regeneration. The decrease in the number of subcutaneous mast cells was accompanied by a parallel reduction of histamine as appreciated by the guinea pig ileum assay. The peripheral vasodilation, which is an early sign of magnesium deficiency, did not appear in rats pretreated with 48/80.

scholarly journals ELECTRON MICROSCOPE OBSERVATIONS ON COMPOUND 48/80-INDUCED DEGRANULATION IN RAT MAST CELLS

1971 ◽  
Vol 51 (2) ◽  
pp. 465-483 ◽  
Author(s):  
Pál Röhlich ◽  
Per Anderson ◽  
Börje Uvnäs
Keyword(s):  
Electron Microscopy ◽  
Mast Cells ◽  
Extracellular Space ◽  
Ultrastructural Changes ◽  
Cell Interior ◽  
Lag Period ◽  
Histamine Liberator ◽  
Granule Matrix ◽  
Rat Mast Cells

In vitro degranulation of rat mast cells was studied at different intervals ranging from 10 to 60 sec after adding the histamine liberator, compound 48/80 (0.4 µg/ml, 17°C). The ultrastructural changes were followed by electron microscopy, and parallel assays were made to determine the histamine released. In addition, the extracellular tracers lanthanum and hemoglobin (demonstrated by its peroxidative activity) were applied to mast cells to follow communication of the extracellular space with the cavities formed during degranulation. After a lag period of 10 sec, degranulation started in the most peripherally located granules. The perigranular membrane fused with the plasma membrane, resulting in a pore bridged by a thin diaphragm. This was followed by rupture of the diaphragm and extrusion of the granule matrix (exocytosis). The process advanced towards the cell interior by fusion and opening of the deeper situated granules to the formerly opened granule cavities. At the end of the process, the cell was filled by a system of complicated cavities containing a number of altered granules. Extracellular tracers have shown that these intracellular cavities were in unbroken communication with the extracellular space from the very beginning of their formation. Both lanthanum and hemoglobin were found to be adsorbed to the limiting membrane of the cavities and bound to altered mast cell granules. In contrast, no tracer substance was present in nondegranulating mast cells. Degranulation of mast cells by compound 48/80 is regarded as a sequential exocytosis, a process similar to that described for some exocrine gland cells. All the "intracellular" cavities, formed by degranulation, were shown to communicate with the extracellular space; consequently, granules lying in these cavities must be considered as biologically extracellular. The present findings support the view that histamine is released from the granule matrix by the extracellular ionic milieu.

Suppression of endotoxin-induced corticosterone secretion in rats by H1-antihistamine

1985 ◽  
Vol 248 (1) ◽  
pp. E26-E30 ◽  
Author(s):  
S. Suzuki ◽  
K. Nakano
Keyword(s):  
Mast Cells ◽  
Intraperitoneal Injection ◽  
Immobilization Stress ◽  
Histamine Level ◽  
Concomitant Increase ◽  
Sharp Reduction ◽  
Peripheral Tissues ◽  
Corticosterone Secretion ◽  
Peritoneal Mast Cells ◽  
Histamine Liberator

Corticosterone (CS) secretion is stimulated in rats by an intraperitoneal injection of bacterial lipopolysaccharide (LPS) or by subjecting the animals to immobilization stress. LPS injection caused a significant increase in the lung histamine level and a sharp reduction in the number of intact peritoneal mast cells. Injection of compound 48/80, a histamine liberator, provoked an increase in the histamine levels of the blood and lung and a decrease in the number of intact peritoneal mast cells with a concomitant increase in CS secretion. Administration of histamine, at a dose of 10 mg/kg, induced a marked increase in CS release. LPS-induced CS secretion was attenuated by pretreatment with an H1-antihistamine, promethazine (PMZ), whereas an H2-antihistamine, metiamide, had no effect. In contrast, PMZ was ineffective on CS release provoked by immobilization stress. These results suggest that LPS-induced CS release is mediated, in part, by histamine released in the peripheral tissues, whereas an immobilization stress-induced increase is not mediated by the amine.

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