Inhibitory Effect of Traxanox Sodium on IgE-Mediated Histamine Release from Passively-Sensitized Mast Cells of the Rat in vitro

1982 ◽  
Vol 68 (4) ◽  
pp. 332-337 ◽  
Author(s):  
Kazuhiro Goto ◽  
Masao Hisadome ◽  
Michio Terasawa
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Inhibitory Effect ◽  
Ige Mediated

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.

Tripterine: A Potential Anti-Allergic Compound

2020 ◽  
Vol 22 (1) ◽  
pp. 159-167
Author(s):  
Bao-Jun Zhu ◽  
Ze-Quan Qian ◽  
Hui-Run Yang ◽  
Ru-Xia Li
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Inflammatory Cells ◽  
Allergic Diseases ◽  
Inhibitory Effect ◽  
Inflammatory Factors ◽  
Peritoneal Mast Cells ◽  
Allergic Effect

Background: Tripterine (TRI), an active monomer in Tripterygium wilfordii, has significant pharmacological activities, such as anti-inflammatory, immunosuppressive and anti-tumor activities. TRI may be used to treat allergic diseases because of its characteristics of immunosuppression. Objective: This study aims to explore the anti-allergic effect of TRI. Methods: It was tested in vivo and in vitro in this study. Results : The results showed that TRI could significantly inhibit histamine release from rat peritoneal mast cells; the inhibitory effect of TRI on histamine release was stronger than that of other known histamine inhibitors such as disodium cromoglyceride. TRI also significantly inhibited systemic anaphylactic shock induced by compound 48/80 and skin allergy induced by IgE, and inhibited the expression of inflammatory factors secreted by Human Mast Cells (HMC-1) induced by Phorbol 12-Myristate 13- Acetate (PMA) and calcium carrier A23187. In the animal model of allergic rhinitis induced by Ovalbumin (OA), the scores of friction, histamine, IgE, inflammatory factors and inflammatory cells decreased after TRI was administered orally or nasally. Conclusions : TRI, as an active immunoregulatory factor, has great potential in the treatment of mast cell-mediated allergic diseases.

scholarly journals IgE-mediated anaphylactic degranulation of isolated human skin mast cells

Blood ◽  
1991 ◽  
Vol 77 (3) ◽  
pp. 569-578 ◽  
Author(s):  
AM Dvorak ◽  
W Massey ◽  
J Warner ◽  
S Kissell ◽  
A Kagey-Sobotka ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Human Skin ◽  
Human Lung ◽  
Lipid Bodies ◽  
Fusion Event ◽  
Electron Microscopic ◽  
Ultrastructural Morphology ◽  
Ige Mediated

Isolated human skin mast cells (HSMC) were prepared and cultured overnight before functional and electron microscopic studies. Mast cell suspensions were examined after stimulation with anti-IgE to produce anaphylactic degranulation or examined in buffer-incubated controls. Histamine release was measured in replicate samples. Control, isolated HSMC studied by electron microscopy were well preserved and fully granulated. Although all granule patterns reported for human mast cells were found, crystal granules were the most prevalent, as is true for HSMC in situ. Individual mast cells containing both crystal and scroll granules occurred. Lipid bodies were rare, as in HSMC in situ. Control, isolated mast cells did not express granule changes associated with either piecemeal degranulation or recovery during wound healing in situ; nor were morphologic changes of anaphylactic degranulation present. Spontaneous histamine release was 0% in control samples. Anaphylactic degranulation of isolated HSMC was accompanied by 24% maximum histamine release and characteristically showed extrusion of altered, membrane-free granules through multiple pores in the plasma membrane to the exterior of the cell. Other morphologic aspects of anaphylactic degranulation, as expressed in isolated human lung mast cells, were also present. These events included granule swelling, fusion, alteration of matrix contents, degranulation channel formation, pore formation, and shedding of granules, membranes, and surface processes. The ultrastructural morphology of isolated HSMC and their IgE-mediated degranulation shows some differences from similar studies of isolated human lung mast cells and of human lung and gut mast cells in biopsy samples. These differences include crystal granules as the predominant granule pattern, minor numbers of lipid bodies, and extrusion of granules during anaphylactic degranulation as characteristic for HSMC. By contrast, isolated human lung and gut mast cells have more scroll granules and particle granules, respectively, and more lipid bodies. In isolated human lung mast cells, anaphylactic degranulation is almost exclusively an intracellular fusion event characterized by the formation of complex degranulation channels within which altered granule matrix materials solubilize. In addition to morphologic differences between mast cells of skin, lung, or gut origin, functional differences have also been reported among mast cells of these organs. The ultrastructural morphology of isolated HSMC is identical to that of skin mast cells in biopsy samples, thereby validating the usefulness of this new source of HSMC for correlative functional and morphologic studies.

scholarly journals Impaired FcϵRI stability, signaling, and effector functions in murine mast cells lacking glycosylphosphatidylinositol-anchored proteins

Blood ◽  
2011 ◽  
Vol 118 (16) ◽  
pp. 4377-4383 ◽  
Author(s):  
Wouter L. W. Hazenbos ◽  
Ping Wu ◽  
Jeffrey Eastham-Anderson ◽  
Taroh Kinoshita ◽  
Eric J. Brown
Keyword(s):  
Mast Cells ◽  
Targeted Disruption ◽  
Potential Therapeutic Target ◽  
Effector Functions ◽  
Ige Mediated ◽  
Interchain Interactions ◽  
Β Chain ◽  
Stimulation Of

Abstract A key event and potential therapeutic target in allergic and asthmatic diseases is signaling by the IgE receptor FcϵRI, which depends on its interactions with Src family kinases (SFK). Here we tested the hypothesis that glycosylphosphatidylinositiol-anchored proteins (GPI-AP) are involved in FcϵRI signaling, based on previous observations that GPI-AP colocalize with and mediate activation of SFK. We generated mice with a hematopoietic cell-specific GPI-AP deficiency by targeted disruption of the GPI biosynthesis gene PigA. In these mice, IgE-mediated passive cutaneous anaphylaxis was largely abolished. PigA-deficient mast cells cultured from these mice showed impaired degranulation in response to stimulation with IgE and antigen in vitro, despite normal IgE binding and antigen-induced FcϵRI aggregation. On stimulation of these cells with IgE and antigen, coprecipitation of the FcϵRI α-chain with the γ-chain and β-chain was markedly reduced. As a result, IgE/antigen–induced FcϵRI-Lyn association and γ-chain tyrosine phosphorylation were both impaired in PigA-deficient cells. These data provide genetic evidence for an unanticipated key role of GPI-AP in FcϵRI interchain interactions and early FcϵRI signaling events, necessary for antigen-induced mast cell degranulation.

scholarly journals The inhibitory effect of 3,3',4,5'-tetrahydroxystilbene, a constituent of Cassia garrettiana, on anti-IgE-induced histamine release from human basophils in vitro.

1991 ◽  
Vol 39 (3) ◽  
pp. 805-807 ◽  
Author(s):  
Yoshihiko INAMORI ◽  
Masafumi OGAWA ◽  
Hiroshi TSUJIBO ◽  
Kimiye BABA ◽  
Mitsugi KOZAWA ◽  
...  
Keyword(s):  
Histamine Release ◽  
Inhibitory Effect ◽  
Human Basophils

scholarly journals IgE-mediated anaphylactic degranulation of isolated human skin mast cells

Blood ◽  
1991 ◽  
Vol 77 (3) ◽  
pp. 569-578 ◽  
Author(s):  
AM Dvorak ◽  
W Massey ◽  
J Warner ◽  
S Kissell ◽  
A Kagey-Sobotka ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Human Skin ◽  
Human Lung ◽  
Lipid Bodies ◽  
Fusion Event ◽  
Electron Microscopic ◽  
Ultrastructural Morphology ◽  
Ige Mediated

Abstract Isolated human skin mast cells (HSMC) were prepared and cultured overnight before functional and electron microscopic studies. Mast cell suspensions were examined after stimulation with anti-IgE to produce anaphylactic degranulation or examined in buffer-incubated controls. Histamine release was measured in replicate samples. Control, isolated HSMC studied by electron microscopy were well preserved and fully granulated. Although all granule patterns reported for human mast cells were found, crystal granules were the most prevalent, as is true for HSMC in situ. Individual mast cells containing both crystal and scroll granules occurred. Lipid bodies were rare, as in HSMC in situ. Control, isolated mast cells did not express granule changes associated with either piecemeal degranulation or recovery during wound healing in situ; nor were morphologic changes of anaphylactic degranulation present. Spontaneous histamine release was 0% in control samples. Anaphylactic degranulation of isolated HSMC was accompanied by 24% maximum histamine release and characteristically showed extrusion of altered, membrane-free granules through multiple pores in the plasma membrane to the exterior of the cell. Other morphologic aspects of anaphylactic degranulation, as expressed in isolated human lung mast cells, were also present. These events included granule swelling, fusion, alteration of matrix contents, degranulation channel formation, pore formation, and shedding of granules, membranes, and surface processes. The ultrastructural morphology of isolated HSMC and their IgE-mediated degranulation shows some differences from similar studies of isolated human lung mast cells and of human lung and gut mast cells in biopsy samples. These differences include crystal granules as the predominant granule pattern, minor numbers of lipid bodies, and extrusion of granules during anaphylactic degranulation as characteristic for HSMC. By contrast, isolated human lung and gut mast cells have more scroll granules and particle granules, respectively, and more lipid bodies. In isolated human lung mast cells, anaphylactic degranulation is almost exclusively an intracellular fusion event characterized by the formation of complex degranulation channels within which altered granule matrix materials solubilize. In addition to morphologic differences between mast cells of skin, lung, or gut origin, functional differences have also been reported among mast cells of these organs. The ultrastructural morphology of isolated HSMC is identical to that of skin mast cells in biopsy samples, thereby validating the usefulness of this new source of HSMC for correlative functional and morphologic studies.

The inhibitory effect of complexes of lidocaine with zinc, copper and cobalt on histamine release from rat mast cells. Further studies

1979 ◽  
Vol 9 (1) ◽  
pp. 65-66 ◽  
Author(s):  
W. Kazimierczak ◽  
K. Bańkowska ◽  
B. Adamas ◽  
Cz. Maśliński
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Inhibitory Effect ◽  
Rat Mast Cells
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