Heparin inhibits histamine release from canine mast cells

1993 ◽  
Vol 264 (4) ◽  
pp. L387-L390 ◽  
Author(s):  
N. Inase ◽  
R. E. Schreck ◽  
S. C. Lazarus
Keyword(s):  
Mast Cells ◽  
Charge Density ◽  
Histamine Release ◽  
Negative Charge ◽  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Similar Inhibitory Effect ◽  
Negative Charge Density

To determine the role of heparin in mast cell exocytosis, we studied the effect of heparin on histamine release induced by compound 48/80 or calcium ionophore A23187 in canine mastocytoma cells (BR). Heparin caused concentration-dependent inhibition of compound 48/80-induced histamine release from mast cells (n = 4; P < 0.05) with a mean inhibitory concentration of 0.14 +/- 0.01 U/ml (mean +/- SE). Mean maximal inhibition was 69.3 +/- 2.0%. In contrast, heparin had no effect on calcium ionophore A23187-induced histamine release. Although benzyl alcohol, a preservative of pharmaceutical heparin, had no effect, purified heparin produced a similar inhibitory effect on compound 48/80-induced histamine release (n = 4; P < 0.05). The inhibitory effect of heparin on histamine release was rapid and was eliminated by washing cells. Dextran sulfate, a polysaccharide with negative charge density, produced a similar inhibitory effect on compound 48/80-induced histamine release (n = 4; P < 0.05). We conclude that heparin inhibits compound 48/80-induced exocytosis in mast cells probably by its negative charge density.

Immunologic mast cell-mediated responses and histamine release are attenuated by heparin

1992 ◽  
Vol 73 (3) ◽  
pp. 1093-1101 ◽  
Author(s):  
J. Lucio ◽  
J. D'Brot ◽  
C. B. Guo ◽  
W. M. Abraham ◽  
L. M. Lichtenstein ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Immunoglobulin E ◽  
Specific Antigen ◽  
Calcium Ionophore ◽  
Intradermal Injection ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Dependent Manner

Heparin has been shown to act as a competitive inhibitor of inositol 1,4,5-triphosphate (InsP3) receptors in various cell types. Because InsP3 is one of the second messengers involved in stimulus-secretion coupling in mast cells, it is possible that heparin may inhibit mast cell-mediated reactions. Therefore, in allergic sheep, we tested this hypothesis in two mast cell-mediated reactions induced by immunologic and nonimmunologic stimuli: immediate cutaneous reaction (ICR) and acute bronchoconstrictor response (ABR). In 12 sheep allergic to Ascaris suum antigen, the surface area of the skin wheal was determined 20 min after intradermal injection (0.05 ml) of increasing concentrations of specific antigen, compound 48/80, and histamine, without and after pretreatment with heparin (100, 300, or 1,000 U/kg i.v.). Antigen, compound 48/80, and histamine produced concentration-dependent increases in ICR. Heparin “partially” inhibited the ICR to antigen and compound 48/80 in a dose-dependent manner without modifying the ICR to histamine. The heparin preservative benzyl alcohol was ineffective. In 11 additional sheep, specific lung resistance was measured before and after inhalation challenges with antigen, compound 48/80, and histamine without and with aerosol heparin pretreatment (1,000 U/kg). Heparin blocked the antigen- and compound 48/80-induced bronchoconstriction without modifying the airway effects of histamine. In isolated human uterine mast cells, heparin inhibited the anti-immunoglobulin E- but not the calcium ionophore- (A23187) induced histamine release. These data suggest that heparin inhibits the ICR and ABR induced by stimuli that produce immunologic and nonimmunologic mast cell degranulation without attenuating the effects of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Immunophenotyping and functional analysis of purified human uterine mast cells

Blood ◽  
1992 ◽  
Vol 79 (3) ◽  
pp. 708-712 ◽  
Author(s):  
CB Guo ◽  
A Kagey-Sobotka ◽  
LM Lichtenstein ◽  
BS Bochner
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Cell Heterogeneity ◽  
Mast Cell Heterogeneity

Abstract Human mast cells have been purified from uterine tissues, and their surface marker profile and function have been evaluated as part of ongoing studies of mast cell heterogeneity. Using a panel of antibodies, purified uterine mast cells (UMC; 81% +/- 7% purity, n = 10) were analyzed by immunofluorescence and flow cytometry for surface expression of various antigens. Consistent with previous analyses of mast cells from other tissues, UMC expressed HLA class I, IgE, c-kit receptor, CD9, CD33, CD43, CD45, and CD54, while CD11a, CD11b, CD14, CD16, CD23, and CD64 were not detected. Unlike other mast cells, UMC expressed CD11c/CD18 (p150,95) and CD32 (Fc gamma RII). Additional antigens not previously studied on mast cells included the selectin LECAM-1 (Leu-8) and several beta 1 and beta 3 integrins; expression of very late activation antigen-4 (VLA-4) (CD49d/CD29), VLA-5 (CD49e/CD29), and the vitronectin receptor (CD51/CD61) was seen. Functional studies showed that treatment of human umbilical vein endothelial cells with interleukin-1 (5 ng/mL for 4 hours) resulted in a twofold to threefold increase in adhesiveness for UMC. Purification procedures did not alter histamine release responses to anti-IgE or the calcium ionophore A23187, and treatment of UMC with an anti-CD32 monoclonal antibody (IV.3) did not induce histamine release or alter anti-IgE-induced release. These data suggest that UMC may possess unique phenotypic characteristics, and support the concept of mast cell heterogeneity.

Mechanisms of Nonimmunological Histamine and Tryptase Release from Human Cutaneous Mast Cells

2000 ◽  
Vol 92 (4) ◽  
pp. 1074-1081 ◽  
Author(s):  
Mette Veien ◽  
Fania Szlam ◽  
Jeannine T. Holden ◽  
Koji Yamaguchi ◽  
Donald D. Denson ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Phospholipase A2 ◽  
Histamine Release ◽  
Phospholipase C ◽  
Cell Activation ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Mast Cell Activation ◽  
Ionophore A23187

Background If mast cells are stimulated they release multiple mediators that delineate markers for immunologic and nonimmunologic reactions; histamine and tryptase are the two best known. Although histamine can be assayed in plasma, it is a nonspecific marker with a very short half-life. Tryptase has a longer half-life, but its release has not been proven to be specific for anaphylaxis. The authors investigated the mechanisms of nonimmunologic histamine release from human cutaneous mast cells to understand the mechanisms of mediator release and to determine whether tryptase was specific for allergic mediated activation. Methods Dispersed mast cell suspensions isolated from neonatal foreskins underwent challenge with vancomycin, calcium ionophore A23187, morphine, and atracurium, and histamine tryptase release was measured. The effects of calcium and magnesium, along with phospholipase C and phospholipase A2 inhibitors, also were investigated. Results Tryptase and histamine both were released by the known nonimmunologic stimuli (pharmacologic agents used in the current study; r2 = 0.6). Furthermore, vancomycin- and atracurium-induced histamine release was calcium dependent. Phospholipase C and phospholipase A2 inhibitors decreased vancomycin-induced histamine release, but not calcium ionophore A23187-induced release. Conclusions Tryptase is not a specific marker of mast cell activation (ie., anaphylaxis), and signaling mechanisms for mast cell activation involve activation of phospholipase C and phospholipase A2 pathways that are also involved in other cellular activation mechanisms.

scholarly journals Immunophenotyping and functional analysis of purified human uterine mast cells

Blood ◽  
1992 ◽  
Vol 79 (3) ◽  
pp. 708-712 ◽  
Author(s):  
CB Guo ◽  
A Kagey-Sobotka ◽  
LM Lichtenstein ◽  
BS Bochner
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Cell Heterogeneity ◽  
Mast Cell Heterogeneity

Human mast cells have been purified from uterine tissues, and their surface marker profile and function have been evaluated as part of ongoing studies of mast cell heterogeneity. Using a panel of antibodies, purified uterine mast cells (UMC; 81% +/- 7% purity, n = 10) were analyzed by immunofluorescence and flow cytometry for surface expression of various antigens. Consistent with previous analyses of mast cells from other tissues, UMC expressed HLA class I, IgE, c-kit receptor, CD9, CD33, CD43, CD45, and CD54, while CD11a, CD11b, CD14, CD16, CD23, and CD64 were not detected. Unlike other mast cells, UMC expressed CD11c/CD18 (p150,95) and CD32 (Fc gamma RII). Additional antigens not previously studied on mast cells included the selectin LECAM-1 (Leu-8) and several beta 1 and beta 3 integrins; expression of very late activation antigen-4 (VLA-4) (CD49d/CD29), VLA-5 (CD49e/CD29), and the vitronectin receptor (CD51/CD61) was seen. Functional studies showed that treatment of human umbilical vein endothelial cells with interleukin-1 (5 ng/mL for 4 hours) resulted in a twofold to threefold increase in adhesiveness for UMC. Purification procedures did not alter histamine release responses to anti-IgE or the calcium ionophore A23187, and treatment of UMC with an anti-CD32 monoclonal antibody (IV.3) did not induce histamine release or alter anti-IgE-induced release. These data suggest that UMC may possess unique phenotypic characteristics, and support the concept of mast cell heterogeneity.

Isolated canine mastocytoma cells: propagation and characterization of two cell lines

1986 ◽  
Vol 251 (6) ◽  
pp. C935-C944 ◽  
Author(s):  
S. C. Lazarus ◽  
R. DeVinney ◽  
L. J. McCabe ◽  
W. E. Finkbeiner ◽  
D. J. Elias ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Cell Lines ◽  
Calcium Ionophore ◽  
Functional Change ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Significant Difference ◽  
Mastocytoma Cells ◽  
Dose Dependent

Five different dog mastocytoma tumors were successfully transplanted and propagated in BALB/c nude mice. Cells from two of these tumors were passaged serially through at least four generations of mice without morphological or functional change. The average yield from a 2-cm tumor harvested from a mouse was 1.2 +/- 2.8 X 10(9) mast cells with greater than 90% viability. Cells of one line were larger and more heavily granulated than the other, and contained 1.29 +/- 0.74 pg histamine/cell (mean +/- SD). Calcium ionophore A23187 and compound 48/80 caused dose dependent histamine release with no significant difference in release from generation to generation. The smaller cells contained 0.06 +/- 0.06 pg histamine/cell. Histamine release after calcium ionophore or compound 48/80 was dose dependent and unchanged through serial passages. Following passive sensitization antigen caused dose-dependent histamine release confirming the presence of IgE receptors on these cells. In both cell lines histamine release was inhibited by terbutaline, dibutyryl adenosine 3',5'-cyclic monophosphate, or isobutylmethylxanthine. These methods provide a morphologically and functionally stable population of nearly pure canine mast cells for biochemical and physiological studies.

Beta-adrenergic and prostanoid inhibition of canine fundic mucosal mast cells

1989 ◽  
Vol 256 (4) ◽  
pp. G727-G732
Author(s):  
A. H. Soll ◽  
M. Toomey
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Cell Activation ◽  
Phosphodiesterase Inhibitor ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Adrenergic Agonists ◽  
Mucosal Mast Cells ◽  
Adrenergic Antagonists

We examined regulation of histamine release from canine hepatic and fundic mucosal mast cells in short-term culture. We found that beta- but not alpha-adrenergic agonists markedly inhibited concanavalin A (ConA)-stimulated histamine release. Inhibition by epinephrine was reversed by the beta-antagonist propranolol, but not by the alpha-adrenergic antagonists phentolamine or yohimbine. The beta 2-selective antagonist ICI 115881 reversed the effects of epinephrine, whereas the beta 1-antagonists practolol and betaxolol had little effect. Prostaglandin E2 (PGE2), but not its analogue enprostil, inhibited ConA-stimulated histamine release. This difference may relate to the ability of PGE2, but not enprostil, to stimulate adenosine 3',5'-cyclic monophosphate (cAMP) production. Forskolin, cAMP analogues, and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine also effectively inhibited ConA-stimulated histamine release. Neither adrenergic agonists nor PGE2 inhibited histamine release stimulated by the combination of phorbol 12-myristate-13-acetate plus the calcium ionophore A23187. These data suggest that inhibition was mediated via cAMP-dependent mechanisms and was exerted on primary cell activation, rather than on postreceptor activating events.

Andalusol, a Diterpenoid with anti-inflammatory Activity from Siderits foetens Clemen

1997 ◽  
Vol 52 (11-12) ◽  
pp. 844-849 ◽  
Author(s):  
A. Navarro ◽  
B. de las Heras
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Calcium Ionophore ◽  
Topical Administration ◽  
Calcium Ionophore A23187 ◽  
Inflammatory Activity ◽  
Specific Marker ◽  
Ionophore A23187 ◽  
Anti Inflammatory

Abstract The anti-inflammatory activity of andalusol (ent-13(16),14-labdadiene-6α,8α,18-triol), a diterpenoid obtained from the acetone extract of Sideritis foetens Clemen, has been investigated. This compound was able to inhibit acute inflammatory processes induced by carrageenan or 12-O -tetradecanoylphorbol acetate (TPA ) after oral or topical administration. Quantitation of the neutrophil specific marker, myeloperoxidase (MPO), demonstrated that its topical anti-inflammatory effect was associated with reduction in neutrophil infiltration into inflamed tissues. Interaction of andalusol with leukocyte functions and histamine release from mast cells was analyzed in vitro. At a concentration of 100 μm andalusol decreased β-glucuronidase release from calcium ionophore A23187-stimulated rat peritoneal leukocytes. However, it failed to affect superoxide generation on TPA -stimulated leukocytes and it was non toxic to leukocytes up to 100 μm (assayed in terms of lactate dehydrogenase release). Andalusol produced a dose-dependent inhibition on histamine release from rat peritoneal mast cells stimulated by com pound 48/80 or calcium ionophore A23187. These results suggest that andalusol possesses an anti-inflammatory profile, and it is in part responsible for the anti-inflammatory activity attributed to this plant.

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