scholarly journals Immunoglobulin E decapeptide-induced 5-hydroxytryptamine release from rat peritoneal mast cells. Comparison with corticotropin-(1–24)-peptide, polyarginine, polylysine and antigen

1981 ◽  
Vol 198 (3) ◽  
pp. 615-619 ◽  
Author(s):  
J W Coleman ◽  
S T Holgate ◽  
M K Church ◽  
R C Godfrey
Keyword(s):  
Mast Cells ◽  
Benzalkonium Chloride ◽  
Immunoglobulin E ◽  
Response Curves ◽  
Low Concentrations ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
High Concentrations ◽  
Concentration Response Curve ◽  
Net Release

A synthetic basic decapeptide from the C4 domain of human immunoglobulin E, corticotropin-(1-24)-peptide, polyarginine and polylysine stimulated up to 90% net release of 5-hydroxytryptamine from mast cells in rat peritoneal-cell suspensions. Concentration-response curves to all four polypeptides were parallel. Polyarginine and polylysine (EC50 congruent to 0.05 microM) were approximately 100-fold more potent than immunoglobulin E decapeptide and corticotropin-(1-24)-peptide (EC50 congruent to 5 microM). Polypeptide-induced release was complete within 5-10s. Immunoglobulin-E-decapeptide-induced 5-hydroxytryptamine release was additive to that induced by low concentrations of polyarginine, but non-additive to that induced by high concentrations of polyarginine. In contrast, release induced by antigen was additive along the whole length of the concentration-response curve to polyarginine. Benzalkonium chloride inhibited immunoglobulin-E-decapeptide- and polyarginine-induced 5-hydroxytryptamine release but enhanced release induced by immunological stimulation.

scholarly journals Evidence for a role of phosphatidylinositol turnover in stimulus–secretion coupling. Studies with rat peritoneal mast cells

1979 ◽  
Vol 178 (3) ◽  
pp. 681-687 ◽  
Author(s):  
Shamshad Cockcroft ◽  
Bastien D. Gomperts
Keyword(s):  
Mast Cells ◽  
Concanavalin A ◽  
Immunoglobulin E ◽  
Histamine Secretion ◽  
Phosphatidylinositol Turnover ◽  
Phosphatidylinositol Response ◽  
Peritoneal Mast Cells ◽  
Stimulus Secretion Coupling ◽  
Rat Peritoneal Mast Cells

Histamine secretion and phosphatidylinositol turnover were compared in antigen-sensitized rat peritoneal mast cells stimulated with a number of different ligands. A small and variable increase in the incorporation of [32P]Pi and of [3H]inositol into phosphatidylinositol was observed when the cells were treated with immunoglobulin E-directed ligands (antigens and concanavalin A), and this was accompanied by a low amount of secretion (<10% of total cell histamine). In the presence of added phosphatidylserine, the addition of immunoglobulin E-directed ligands invariably led to an enhanced rate (approx. 4-fold) of labelling of phosphatidylinositol and, in the presence of Ca2+, this was accompanied by the secretion of histamine. The labelling of phosphatidylinositol and histamine secretion were also stimulated by chymotrypsin and compound 48/80. Whereas the phosphatidylinositol response did not require the presence of extracellular Ca2+, the secretion of histamine was either enhanced or dependent on extracellular Ca2+ (depending on the ligand used). The dependence on ligand concentration for the phosphatidylinositol response and histamine secretion were similar. The increased isotopic incorporation into phosphatidylinositol continued for about 1h although histamine secretion (elicited with concanavalin A) stopped within 2min. These results support the proposition that metabolic events involving phosphatidylinositol play a necessary intermediate role in the regulation of Ca2+ channels by ligand-activated receptors.

Effects of Siegesbeckia pubescens on Immediate Hypersensitivity Reaction

1997 ◽  
Vol 25 (02) ◽  
pp. 163-167 ◽  
Author(s):  
Hyung Min Kim
Keyword(s):  
Mast Cells ◽  
Hypersensitivity Reaction ◽  
Histamine Release ◽  
Immunoglobulin E ◽  
Immediate Hypersensitivity ◽  
Antiallergic Activity ◽  
Peritoneal Mast Cells ◽  
Ige Mediated ◽  
Rat Peritoneal Mast Cells ◽  
Siegesbeckia Pubescens

This study was carried out to examine the effect of an aqueous extract from Siegesbeckia pubescens (Compositae) (SPAE) on immunoglobulin E (IgE)-mediated immediate hypersensitivity reaction. Forty-eight hours passive cutaneous anaphylaxis in rats was significantly inhibited by oral administration of SPAE (100 μg/g). It also inhibited histamine release from rat peritoneal mast cells induced by anti-dinitrophenyl (DNP)-IgE and DNP-human serum albumin. The data indicate that SPAE has antiallergic activity, and that its action may be due to inhibition of histamine release from mast cells.

Inhibitors of the arachidonic acid cascade dissociate 48/80-induced Ca2+ influx and Ca2+ release in mast cells

1993 ◽  
Vol 264 (4) ◽  
pp. C912-C917 ◽  
Author(s):  
M. Kuno ◽  
J. Kawawaki ◽  
T. Shibata ◽  
H. Gotani
Keyword(s):  
Arachidonic Acid ◽  
Mast Cells ◽  
Nordihydroguaiaretic Acid ◽  
Arachidonic Acid Cascade ◽  
Lipoxygenase Inhibitor ◽  
Low Concentrations ◽  
Peritoneal Mast Cells ◽  
Stimulus Secretion Coupling ◽  
Rat Peritoneal Mast Cells ◽  
Full Activation

Effects of inhibitors of the arachidonic acid cascade on Ca2+ release from intracellular stores and Ca2+ influx through the plasma membrane during stimulus-secretion coupling were examined using rat peritoneal mast cells loaded with fura-2. Compound 48/80 (48/80) was used as a secretagogue. A phospholipase inhibitor, p-bromophenacyl bromide (PBPB), or a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), inhibited the 48/80 (1 microgram/ml)-induced release of histamine, Ca2+, and Mn2+ influxes, but the cyclooxygenase inhibitor, indomethacin (approximately 50 microM), inhibited neither Ca2+ nor Mn2+ influxes. The Ca2+ release induced by 1 microgram/ml of 48/80 was little inhibited by PBPB, NDGA, or indomethacin. The Ca2+ release was activated and saturated with lower concentrations of 48/80 than was the Ca2+ influx. The percent inhibition of the Ca2+ release by 25 microM PBPB was increased by lowering the concentration of 48/80, but NDGA (10 microM) did not inhibit the Ca2+ release induced by low concentrations of 48/80 (0.03-0.1 microgram/ml). These results suggest that activation of the Ca2+ release and the Ca2+ influx were differently regulated and that full activation of Ca2+ influx needs the arachidonic acid cascade produced by higher concentrations of 48/80 than does the Ca2+ release. Lipoxygenase metabolites of arachidonic acid are potential modulators of the Ca2+ influx.

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