The Inhibitory Effect of Nicotinamide on Asthma-Like Symptoms and Eosinophilia in Guinea Pigs, Anaphylactic Mast Cell Degranulation in Mice, and Histamine Release from Rat Isolated Peritoneal Mast Cells by Compound 48/80

1974 ◽  
Vol 47 (5) ◽  
pp. 737-748 ◽  
Author(s):  
Estera Bekier ◽  
Janina Wyczółkowska ◽  
Hanna Szyc ◽  
Cz. Maśliński
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Guinea Pigs ◽  
Inhibitory Effect ◽  
Mast Cell Degranulation ◽  
Peritoneal Mast Cells

Dural mast cell degranulation is a putative mechanism for headache induced by PACAP-38

Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Michael Baun ◽  
Martin Holst Friborg Pedersen ◽  
Jes Olesen ◽  
Inger Jansen-Olesen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Adenylate Cyclase ◽  
Phospholipase C ◽  
Dura Mater ◽  
Mast Cell Degranulation ◽  
Peritoneal Mast Cell ◽  
Selective Blockade ◽  
Peritoneal Mast Cells

Background: Pituitary adenylate cyclase activating peptide-38 (PACAP-38) has been shown to induce migraine in migraineurs, whereas the related peptide vasoactive intestinal peptide (VIP) does not. In the present study we examine the hypothesis that PACAP-38 and its truncated version PACAP-27 but not VIP cause degranulation of mast cells in peritoneum and in dura mater. Methods: The degranulatory effects of PACAP-38, PACAP-27 and VIP were investigated by measuring the amount of N-acetyl-β-hexosaminidase released from isolated peritoneal mast cells and from dura mater attached to the skull of the rat in vitro. In peritoneal mast cells N-truncated fragments of PACAP-38 (PACAP(6–38), PACAP(16–38) and PACAP(28–38)) were also studied. To investigate transduction pathways involved in mast cell degranulation induced by PACAP-38, PACAP-27 and VIP, the phospholipase C inhibitor U-73122 and the adenylate cyclase inhibitor SQ 22536 were used. Results: The peptides induced degranulation of isolated peritoneal mast cells of the rat with the following order of potency: PACAP-38 = PACAP(6–38) = PACAP(16–38) » PACAP-27 = VIP = PACAP(28–38). In the dura mater we found that 10−5 M PACAP-38 was significantly more potent in inducing mast cell degranulation than the same concentration of PACAP-27 or VIP. Inhibition of intracellular mechanisms demonstrated that PACAP-38-induced degranulation is mediated by the phospholipase C pathway. Selective blockade of the PAC1 receptor did not attenuate degranulation. Conclusion: These findings correlate with clinical studies and support the hypothesis that mast cell degranulation is involved in PACAP-induced migraine. PACAP-38 has a much stronger degranulatory effect on rat peritoneal and dural mast cells than VIP and PACAP-27. The difference in potency between PACAP-38- and PACAP-27/VIP-induced peritoneal mast cell degranulation is probably not related to the PAC1 receptor but is caused by a difference in efficacy on phospholipase C.

Aqueous Extract of Mosla chinensis Inhibits Mast Cell-Mediated Allergic Inflammation

2012 ◽  
Vol 40 (06) ◽  
pp. 1257-1270 ◽  
Author(s):  
Hui-Hun Kim ◽  
Jin-Su Yoo ◽  
Tae-Yong Shin ◽  
Sang-Hyun Kim
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Aqueous Extract ◽  
Proinflammatory Cytokines ◽  
Immunoglobulin E ◽  
Inflammatory Diseases ◽  
Allergic Inflammation ◽  
Inhibitory Effect ◽  
Ige Mediated

Allergic inflammatory diseases such as food allergy, asthma, sinusitis, and atopic dermatitis are increasing worldwide. In this study, we investigated the effects of aqueous extract of Mosla chinensis Max. (AMC) on mast cell-mediated allergic inflammation and studied the possible mechanism of this action. AMC inhibited compound 48/80-induced systemic and immunoglobulin E (IgE)-mediated local anaphylaxis. AMC reduced intracellular calcium levels and downstream histamine release from rat peritoneal mast cells activated by compound 48/80 or IgE. In addition, AMC decreased gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 in human mast cells. The inhibitory effect of AMC on cytokine expression was nuclear factor (NF)-κB dependent. Our results indicate that AMC inhibits mast cell-mediated allergic inflammatory reaction by suppressing histamine release and expression of proinflammatory cytokines and the involvement of calcium and NF-κB in these effects. AMC might be a possible therapeutic candidate for allergic inflammatory disorders.

Inhibition of Mast Cell-Mediated Anaphylaxis by Sochungryong-Tang

2000 ◽  
Vol 28 (01) ◽  
pp. 69-76 ◽  
Author(s):  
H. M. Kim ◽  
G. S. Yoon ◽  
J. U. Seo ◽  
G. Moon ◽  
H. R. Kim ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Anaphylactic Shock ◽  
Mast Cell Degranulation ◽  
Dependent Manner ◽  
Asian Philosophy ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Anti Body ◽  
Dose Dependent

According to traditional Asian philosophy, Sochungryong-Tang (S-Tang) is a prescription for treating exterior syndrome. In this study, we investigated the effect of S-Tang on mast cell-mediated anaphylaxis. S-Tang completely inhibited compound 48/80-induced systemic anaphylactic shock at a dose of 100 mg/kg. When S-Tang was given as pretreatment at concentrations ranging from 1 to 1000 mg/kg, the serum histamine levels induced by compound 48/80 were reduced in a dose-dependent manner. S-Tang inhibited the local anaphylaxis activated by anti-dinitrophenyl (DNP) IgE anti-body, and also inhibited the histamine release from the rat peritoneal mast cells by compound 48/80 or anti-DNP IgE. These results indicate that S-Tang may contain substances with actions that inhibit mast cell degranulation.

scholarly journals Anti-immunoglobulin-induced histamine secretion by rat peritoneal mast cells studied by immunoferritin electron microscopy.

1975 ◽  
Vol 142 (2) ◽  
pp. 391-402 ◽  
Author(s):  
D Lawson ◽  
C Fewtrell ◽  
B Gomperts ◽  
M Raff
Keyword(s):  
Electron Microscopy ◽  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Histamine Secretion ◽  
Calcium Dependent ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells

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.

scholarly journals ANTIGEN-INDUCED RELEASE OF SLOW REACTING SUBSTANCE OF ANAPHYLAXIS (SRS-ARAT) IN RATS PREPARED WITH HOMOLOGOUS ANTIBODY

1968 ◽  
Vol 127 (4) ◽  
pp. 767-782 ◽  
Author(s):  
Robert P. Orange ◽  
Martin D. Valentine ◽  
K. Frank Austen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Reaction Sequence ◽  
Peritoneal Mast Cells ◽  
Pmn Leukocytes ◽  
Circulating Lymphocytes ◽  
Pharmacologic Inhibitors ◽  
Antigen Antibody ◽  
Marked Suppression

The polymorphonuclear leukocyte appears to be an essential cellular prerequisite for the antigen-induced release of SRS-Arat in the peritoneal cavity of rats prepared with homologous, hyperimmune antisera. Depletion of PMN leukocytes is associated with a marked suppression of SRS-Arat release, whereas depletion of circulating lymphocytes or peritoneal mast cells does not influence the antigen-induced release of SRS-Arat. A local increase in the number of PMN leukocytes produced by the induction of a peritoneal exudate was associated with an enhanced release of SRS-Arat. A distinct difference in the cellular requirements for the antigen-induced release of histamine and SRS-Arat in the rat was observed. Homocytotropic antibody-mediated histamine release could be achieved in leukopenic rats but not in mast cell-depleted animals. Conversely, SRS-Arat release was suppressed in leukopenic rats but was unaffected by mast cell depletion. Diethylcarbamazine inhibited the antigen-induced release of SRS-Arat following preparation with homologous, hyperimmune antisera but did not interfere with homocytotropic antibody-mediated histamine release. In preventing SRS-Arat release, diethylcarbamazine did not interfere with antigen-antibody interaction since desensitization of tissues was possible in the presence of this inhibitor. This observation is consistent with the view that diethylcarbamazine inhibits the reaction sequence leading to the formation and release of SRS-Arat at some step subsequent to antigen-antibody interaction. These studies support the view that the immunologic pathways leading to the release of SRS-Arat and histamine in the rat are distinctly different in terms of the immunoglobulins involved, the cellular prerequisites, and the effective pharmacologic inhibitors.

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