scholarly journals Potential prophylactic efficacy of mast cell stabilizers against COVID-19 vaccine-induced anaphylaxis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Itsuro Kazama
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Allergic Reactions ◽  
Prophylactic Efficacy ◽  
First Choice ◽  
Systemic Side Effects ◽  
Sudden Release ◽  
Prophylactic Use ◽  
Basic Studies ◽  
Chemical Mediators

AbstractTo fight against coronavirus disease 2019 (COVID-19), the vaccination is currently the most effective approach. However, in addition to common systemic side effects, the vaccines can cause serious allergic reactions or anaphylaxis. In anaphylaxis, the exposure to the allergen causes a sudden release of chemical mediators from mast cells, for which adrenaline is the drug of first choice. In our previous basic studies, in addition to adrenaline, anti-allergic drugs (olopatadine, loratadine, tranilast and ketotifen), antibiotics (clarithromycin), corticosteroids (hydrocortisone and dexamethasone) and certain food constituents (caffeine and catechin) inhibited the process of exocytosis and showed their effectiveness as highly potent mast cell stabilizers. In these studies, since mast cells were pre-incubated with these drugs or the food constituents before exocytosis was induced, the findings strongly indicated their prophylactic efficacy in stabilizing mast cells. Considering such pharmacological properties of these commonly prescribed medications or the food constituents, their prophylactic use may potentially be beneficial in preventing anaphylaxis caused by COVID-19 vaccination.

scholarly journals Preventative and Therapeutic Effects of Low-dose Ionizing Radiation on the Allergic Response of Rat Basophilic Leukemia Cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hae Mi Joo ◽  
Eun Hee Hong ◽  
Seong-Jun Cho ◽  
Seon Young Nam ◽  
Ji Young Kim
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Ionizing Radiation ◽  
Therapeutic Effect ◽  
Cell Activation ◽  
Low Dose ◽  
Mast Cell Activation ◽  
Allergic Reactions ◽  
Antigen Antibody ◽  
Basophilic Leukemia

Abstract The prevalence of allergies has increased over the last four decades. In allergic reactions, mast cells induce a hypersensitive immune response to a substance that is normally harmless. Ionizing radiation has different biological effects depending on the dose and dose rate. In this study, we investigated whether low-dose irradiation before (preventative effect) or after (therapeutic effect) an antigen-antibody reaction has an anti-allergic effect. To test this, we activated rat basophilic leukemia (RBL-2H3) mast cells with anti-2,4-dinitrophenyl IgE (antibody) and 2,4-dinitrophenyl human serum albumin, which served as an antigen. To test for both the potential of a preventative effect and a therapeutic effect, we irradiated mast cells both before and after mast cell activation, and we measured mediator release and signaling pathway activity. Low-dose ionizing radiation suppressed mediator release from RBL-2H3 mast cells activated by the antigen-antibody reaction regardless of when the mast cells were irradiated. These results were due to the suppression of FcεRI expression. Therefore, we suggest that low-dose ionizing radiation has a preventative and therapeutic effect in allergic reactions via the FcεRI-mediated RBL-2H3 mast cell activation system.

scholarly journals Ethanol Extract of Sesamum indicum Linn. Inhibits FcεRI-Mediated Allergic Reaction via Regulation of Lyn/Syk and Fyn Signaling Pathways in Rat Basophilic Leukemic RBL-2H3 Mast Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Hyun Ju Do ◽  
Tae Woo Oh ◽  
Kwang-Il Park
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Signaling Pathways ◽  
Inflammatory Mediators ◽  
Cell Activation ◽  
Immunoglobulin E ◽  
Sesamum Indicum ◽  
Mast Cell Activation ◽  
Allergic Reactions ◽  
Potent Effect

This study is aimed at determining whether Sesamum indicum Linn. beneficially influences FcεRI-mediated allergic reactions in RBL-2H3 mast cells; it is also aimed at further investigating Lyn/Fyn and Syk signaling pathways. To examine the antiallergic effect of Sesamum indicum Linn. extract (SIE), we treated antigen/immunoglobulin E- (IgE-) sensitized mast cells with extracts of various concentrations. We examined the degranulation release and concentrations of inflammatory mediators. Additionally, the expressions of genes involved in the FcεRI and arachidonate signaling pathways were examined. SIE inhibited the degranulation and secretion of inflammatory mediators in antigen/IgE-sensitized mast cells. SIE reduced the expressions of FcεRI signaling-related genes, such as Syk, Lyn, and Fyn, and the phosphorylation of extracellular signal-regulated kinase in antigen/IgE-sensitized mast cells. Additionally, in late allergic responses, SIE reduced PGD2 release and COX-2 and cPLA2 phosphorylation expression in FcεRI-mediated mast cell activation. Lastly, 250–500 mg/kg SIE significantly attenuated the Ag/IgE-induced passive cutaneous anaphylaxis (PCA) reaction in mice. The potent effect of SIE on RBL-2H3 mast cell activation indicates that the extract could potentially be used as a novel inhibitor against allergic reactions.

scholarly journals Tespa1 negatively regulates FcεRI-mediated signaling and the mast cell–mediated allergic response

2014 ◽  
Vol 211 (13) ◽  
pp. 2635-2649 ◽  
Author(s):  
Di Wang ◽  
Mingzhu Zheng ◽  
Yuanjun Qiu ◽  
Chuansheng Guo ◽  
Jian Ji ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Cytokine Production ◽  
Adaptor Protein ◽  
Mast Cell Activation ◽  
Allergic Reactions ◽  
Proinflammatory Cytokine Production ◽  
Increased Sensitivity ◽  
Ige Mediated

Antigen-mediated cross-linking of IgE on mast cells triggers a signaling cascade that results in their degranulation and proinflammatory cytokine production, which are key effectors in allergic reactions. We show that the activation of mast cells is negatively regulated by the newly identified adaptor protein Tespa1. Loss of Tespa1 in mouse mast cells led to hyper-responsiveness to stimulation via FcεRI. Mice lacking Tespa1 also displayed increased sensitivity to IgE-mediated allergic responses. The dysregulated signaling in KO mast cells was associated with increased activation of Grb2-PLC-γ1-SLP-76 signaling within the LAT1 (linker for activation of T cells family, member 1) signalosome versus the LAT2 signalosome. Collectively, these findings show that Tespa1 orchestrates mast cell activation by tuning the balance of LAT1 and LAT2 signalosome assembly.

scholarly journals Killer Immunoglobulin-Like Receptor 2DL4 (CD158d) Regulates Human Mast Cells Both Positively and Negatively: Possible Roles in Pregnancy and Cancer Metastasis

2019 ◽  
Author(s):  
Tatsuki R. Kataoka ◽  
Chiyuki Ueshima ◽  
Masahiro Hirata ◽  
Sachiko Minamiguchi ◽  
Hironori Haga
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cancer Metastasis ◽  
Nk Cell ◽  
Human Leukocyte ◽  
Human Mast Cell ◽  
Allergic Reactions ◽  
Ige Receptor ◽  
Human Mast Cells ◽  
In Pregnancy

Killer immunoglobulin-like receptor (KIR) 2DL4 (CD158d) was previously thought to be a human NK-cell-specific protein but its expression has also been demonstrated in human mast cells. Mast cells are involved in allergic reactions via their KIT-mediated and IgE receptor-mediated responses. We recently detected the expression of KIR2DL4 in human cultured mast cells established from peripheral blood derived from healthy volunteers (PB-mast), a human mast cell line (LAD2), and non-neoplastic mast cells, including pathological specimens. An agonistic antibody against KIR2DL4 negatively regulates the KIT- and IgE-receptor-mediated responses of PB-mast and LAD2 cells. In addition, agonistic antibodies and human leukocyte antigen (HLA)-G, a natural ligand for KIR2DL4, induce the secretion from these cells of leukemia inhibitory factor and serine proteases, which have been implicated in pregnancy establishment and cancer metastasis. Therefore, KIR2DL4 stimulation with agonistic antibodies and recombinant HLA-G protein may enhance both processes, in addition to suppressing mast-cell-mediated allergic reactions.

scholarly journals Neutrophil serine protease 4 is required for mast cell-dependent vascular leakage

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Andrew P. AhYoung ◽  
Sterling C. Eckard ◽  
Alvin Gogineni ◽  
Hongkang Xi ◽  
S. Jack Lin ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Serine Protease ◽  
Mouse Models ◽  
Vascular Leakage ◽  
Allergic Reactions ◽  
Acute Arthritis ◽  
Sustained Reduction ◽  
Granule Morphology ◽  
Deficient Mice

AbstractVascular leakage, or edema, is a serious complication of acute allergic reactions. Vascular leakage is triggered by the release of histamine and serotonin from granules within tissue-resident mast cells. Here, we show that expression of Neutrophil Serine Protease 4 (NSP4) during the early stages of mast cell development regulates mast cell-mediated vascular leakage. In myeloid precursors, the granulocyte–macrophage progenitors (GMPs), loss of NSP4 results in the decrease of cellular levels of histamine, serotonin and heparin/heparan sulfate. Mast cells that are derived from NSP4-deficient GMPs have abnormal secretory granule morphology and a sustained reduction in histamine and serotonin levels. Consequently, in passive cutaneous anaphylaxis and acute arthritis models, mast cell-mediated vascular leakage in the skin and joints is substantially reduced in NSP4-deficient mice. Our findings reveal that NSP4 is required for the proper storage of vasoactive amines in mast cell granules, which impacts mast cell-dependent vascular leakage in mouse models of immune complex-mediated diseases.

scholarly journals Transgenic mice expressing the human high-affinity immunoglobulin (Ig) E receptor alpha chain respond to human IgE in mast cell degranulation and in allergic reactions.

1996 ◽  
Vol 183 (1) ◽  
pp. 49-56 ◽  
Author(s):  
W P Fung-Leung ◽  
J De Sousa-Hitzler ◽  
A Ishaque ◽  
L Zhou ◽  
J Pang ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Transgenic Mice ◽  
Cell Activation ◽  
Surface Expression ◽  
Mast Cell Activation ◽  
Cell Surface Expression ◽  
Allergic Reactions ◽  
Alpha Chain ◽  
Ige Mediated

The high-affinity receptor for immunoglobulin (Ig) E (Fc epsilon RI) on mast cells and basophils plays a key role in IgE-mediated allergies. Fc epsilon RI is composed of one alpha, one beta, and two gamma chains, which are all required for cell surface expression of Fc epsilon RI, but only the alpha chain is involved in the binding to IgE. Fc epsilon RI-IgE interaction is highly species specific, and rodent Fc epsilon RI does not bind human IgE. To obtain a "humanized" animal model that responds to human IgE in allergic reactions, transgenic mice expressing the human Fc epsilon RI alpha chain were generated. The human Fc epsilon RI alpha chain gene with a 1.3-kb promoter region as a transgene was found to be sufficient for mast cell-specific transcription. Cell surface expression of the human Fc epsilon RI alpha chain was indicated by the specific binding of human IgE to mast cells from transgenic mice in flow cytometric analyses. Expression of the transgenic Fc epsilon RI on bone marrow-derived mast cells was 4.7 x 10(4)/cell, and the human IgE-binding affinity was Kd = 6.4 nM in receptor-binding studies using 125I-IgE. The transgenic human Fc epsilon RI alpha chain was complexed with the mouse beta and gamma chains in immunoprecipitation studies. Cross-linking of the transgenic Fc epsilon RI with human IgE and antigens led to mast cell activation as indicated by enhanced tyrosine phosphorylation of the Fc epsilon RI beta and gamma chains and other cellular proteins. Mast cell degranulation in transgenic mice could be triggered by human IgE and antigens, as demonstrated by beta-hexosaminidase release in vitro and passive cutaneous anaphylaxis in vivo. The results demonstrate that the human Fc epsilon RI alpha chain alone not only confers the specificity in human IgE binding, but also can reconstitute a functional receptor by coupling with the mouse beta and gamma chains to trigger mast cell activation and degranulation in a whole animal system. These transgenic mice "humanized" in IgE-mediated allergies may be valuable for development of therapeutic agents that target the binding of IgE to its receptor.

Inhibitory Effects of BiRyuChe-Bang on Mast Cell-Mediated Allergic Reactions and Inflammatory Cytokines Production

2013 ◽  
Vol 41 (06) ◽  
pp. 1267-1282 ◽  
Author(s):  
Phil-Dong Moon ◽  
Il Sang Choi ◽  
Ji-Hyun Go ◽  
Byong-Joo Lee ◽  
Sang Woo Kang ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Inflammatory Cytokines ◽  
Medical Center ◽  
Human Mast Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Allergic Reactions ◽  
Linalyl Acetate ◽  
Tnf Α

BiRyuChe-bang (BRC) is a Korean prescription medicine, which has been used to treat allergic rhinitis at Kyung Hee Medical Center. In this work, we investigated the effects of BRC on mast cell-mediated allergic reactions and inflammatory cytokines production, and identified the active component of BRC. Histamine release was measured from rat peritoneal mast cells (RPMCs). Ear swelling and passive cutaneous anaphylaxis (PCA) were examined in mouse models. Phorbol 12-myristate 13-acetate (PMA) plus A23187-induced inflammatory cytokines production was measured using enzyme-linked immunosorbent assay. Reverse transcriptase-polymerase chain reaction was used for the expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8. Activation of nuclear factor (NF)-κB was analyzed by Western blotting. BRC significantly inhibited the compound 48/80-induced ear swelling response, histamine release from RPMCs, PCA activated by anti-dinitrophenyl IgE, and PMA plus A23187-induced inflammatory cytokines production (p < 0.05). In addition, BRC dose-dependently inhibited the mRNA expressions of TNF-α, IL-6, and IL-8 as well as the activation of NF-κB in a human mast cell line, HMC-1 cells. BRC inhibited the levels of TNF-α and IL-6 in mice induced with PCA. Several components of BRC, such as 1,8-Cineole, Linalool, Linalyl acetate, α-Pinene, and α-Terpineol, significantly inhibited the release of histamine from RPMCs (p < 0.05). Among these components, Linalyl acetate was the most effective for inhibiting histamine release. These results indicate that BRC has a potential regulatory effect on allergic and inflammatory reactions mediated by mast cells.

Amomum xanthiodes Inhibits Mast Cell-Mediated Allergic Reactions Through the Inhibition of Histamine Release and Inflammatory Cytokine Production

2005 ◽  
Vol 230 (9) ◽  
pp. 681-687 ◽  
Author(s):  
Sang-Hyun Kim ◽  
Tae-Yong Shin
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Proinflammatory Cytokines ◽  
Immunoglobulin E ◽  
Ionophore A23187 ◽  
Allergic Reactions ◽  
Disodium Cromoglycate ◽  
Plasma Histamine ◽  
Intracellular Ca

In this study, we investigated the effect of Amomum xanthiodes (Zingiberaceae) extract (AXE) on the mast cell-mediated allergy model and studied the possible mechanism of action. We found that AXE inhibited compound 48/80-induced systemic reactions and plasma histamine release in mice. Additionally, AXE decreased immunoglobulin E (IgE)-mediated local allergic reactions and passive cutaneous anaphylaxis (PCA), and AXE dose-dependently attenuated the release of histamine from rat peritoneal mast cells (RPMC) activated by compound 48/80 or IgE. The amounts of AXE needed for inhibition of compound 48/80-induced plasma histamine release and PCA were similar to disodium cromoglycate, the known anti-allergic drug. We found that AXE increased the cAMP levels and decreased the compound 48/80-induced intracellular Ca2+. Furthermore, AXE attenuated the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187)-stimulated tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 secretion in human mast cells. The inhibitory effect of AXE on the proinflammatory cytokines was nuclear factor-κB (NF-κB)-dependent. In addition, AXE decreased PMA plus A23187-induced degradation of IκBα and the nuclear translocation of NF-κB. Our findings provide evidence that AXE inhibits mast cell-derived immediate-type allergic reactions, and that cAMP, intracellular Ca2+, proinflammatory cytokines, and NF-κB are involved in these effects.

scholarly journals Killer Immunoglobulin-Like Receptor 2DL4 (CD158d) Regulates Human Mast Cells both Positively and Negatively: Possible Roles in Pregnancy and Cancer Metastasis

2020 ◽  
Vol 21 (3) ◽  
pp. 954 ◽  
Author(s):  
Tatsuki R. Kataoka ◽  
Chiyuki Ueshima ◽  
Masahiro Hirata ◽  
Sachiko Minamiguchi ◽  
Hironori Haga
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Serine Proteases ◽  
Cancer Metastasis ◽  
Nk Cell ◽  
Human Leukocyte ◽  
Human Mast Cell ◽  
Allergic Reactions ◽  
Human Mast Cells ◽  
In Pregnancy

Killer immunoglobulin-like receptor (KIR) 2DL4 (CD158d) was previously thought to be a human NK cell-specific protein. Mast cells are involved in allergic reactions via their KIT-mediated and FcɛRI-mediated responses. We recently detected the expression of KIR2DL4 in human cultured mast cells established from peripheral blood of healthy volunteers (PB-mast), in the human mast cell line LAD2, and in human tissue mast cells. Agonistic antibodies against KIR2DL4 negatively regulate the KIT-mediated and FcɛRI-mediated responses of PB-mast and LAD2 cells. In addition, agonistic antibodies and human leukocyte antigen (HLA)-G, a natural ligand for KIR2DL4, induce the secretion of leukemia inhibitory factor and serine proteases from human mast cells, which have been implicated in pregnancy establishment and cancer metastasis. Therefore, KIR2DL4 stimulation with agonistic antibodies and recombinant HLA-G protein may enhance both processes, in addition to suppressing mast-cell-mediated allergic reactions.

scholarly journals IgE- and IgE+Ag-mediated mast cell migration in an autocrine/paracrine fashion

Blood ◽  
2005 ◽  
Vol 105 (8) ◽  
pp. 3222-3229 ◽  
Author(s):  
Jiro Kitaura ◽  
Tatsuya Kinoshita ◽  
Masaaki Matsumoto ◽  
Shaun Chung ◽  
Yuko Kawakami ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Migration ◽  
Mast Cells ◽  
Tyrosine Kinases ◽  
Immunoglobulin E ◽  
Leukotriene B4 ◽  
Allergic Reactions ◽  
Effector Cells ◽  
Mucosal Tissues ◽  
Paracrine Secretion

AbstractMast cells are the major effector cells for immediate hypersensitivity and chronic allergic reactions. These cells accumulate in mucosal tissues of allergic reactions, where immunoglobulin E (IgE) is produced locally. Here we provide evidence that, in addition to antigen that can attract IgE-bound mast cells, the type of IgE molecules that efficiently activate mast cells can promote the migration of mast cells in the absence of antigen. IgE- and IgE+Ag-mediated migration involves an autocrine/paracrine secretion of soluble factors including adenosine, leukotriene B4, and several chemokines. Their secretion depends on 2 tyrosine kinases, Lyn and Syk, and they are agonists of G-protein-coupled receptors and signal through phosphatidylinositol 3-kinase γ, leading to mast cell migration. In mouse experiments, naive mast cells are attracted to IgE, and IgE-sensitized mast cells are attracted to antigen. Therefore, IgE and antigen are implicated in mast cell accumulation at allergic tissue sites with local high IgE levels. (Blood. 2005;105:3222-3229)

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