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Teruhisa Miike - One of the best experts on this subject based on the ideXlab platform.
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Systemic Anaphylaxis after eating storage-mite-contaminated food.
International Archives of Allergy and Immunology, 1996Co-Authors: Tomoaki Matsumoto, Takeshi Hisano, Masamichi Hamaguchi, Teruhisa MiikeAbstract:We describe 2 cases in whom Systemic Anaphylaxis developed shortly after they had eaten food contaminated by a storage mite, Tyrophagus putrescentiae. We were able to demonstrate that these cases were sensitive to the storage mites but not to food allergens, leading us to conclude that the cases' anaphylactic episodes were the result of ingestion of the storage mites. This is the first report of the ingestion of storage mites causing Systemic Anaphylaxis in sensitive persons.
Hajime Karasuyama - One of the best experts on this subject based on the ideXlab platform.
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Mouse and human neutrophils induce Anaphylaxis.
Journal of Clinical Investigation, 2011Co-Authors: Friederike Jönsson, Hajime Karasuyama, Takao Shimizu, David Mancardi, Yoshihiro Kita, Bruno Iannascoli, Nico Van Rooijen, Marc Daëron, Pierre BruhnsAbstract:Anaphylaxis is a life-threatening hyperacute immediate hypersensitivity reaction. Classically, it depends on IgE, FcεRI, mast cells, and histamine. However, Anaphylaxis can also be induced by IgG antibodies, and an IgG1-induced passive type of Systemic Anaphylaxis has been reported to depend on basophils. In addition, it was found that neither mast cells nor basophils were required in mouse models of active Systemic Anaphylaxis. Therefore, we investigated what antibodies, receptors, and cells are involved in active Systemic Anaphylaxis in mice. We found that IgG antibodies, FcγRIIIA and FcγRIV, platelet-activating factor, neutrophils, and, to a lesser extent, basophils were involved. Neutrophil activation could be monitored in vivo during Anaphylaxis. Neutrophil depletion inhibited active, and also passive, Systemic Anaphylaxis. Importantly, mouse and human neutrophils each restored Anaphylaxis in Anaphylaxis-resistant mice, demonstrating that neutrophils are sufficient to induce Anaphylaxis in mice and suggesting that neutrophils can contribute to Anaphylaxis in humans. Our results therefore reveal an unexpected role for IgG, IgG receptors, and neutrophils in Anaphylaxis in mice. These molecules and cells could be potential new targets for the development of Anaphylaxis therapeutics if the same mechanism is responsible for Anaphylaxis in humans.
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mouse and human neutrophils induce Anaphylaxis
Journal of Clinical Investigation, 2011Co-Authors: Friederike Jönsson, Hajime Karasuyama, Takao Shimizu, David Mancardi, Yoshihiro Kita, Bruno Iannascoli, Nico Van Rooijen, Marc Daëron, Pierre BruhnsAbstract:Anaphylaxis is a life-threatening hyperacute immediate hypersensitivity reaction. Classically, it depends on IgE, FceRI, mast cells, and histamine. However, Anaphylaxis can also be induced by IgG antibodies, and an IgG1-induced passive type of Systemic Anaphylaxis has been reported to depend on basophils. In addition, it was found that neither mast cells nor basophils were required in mouse models of active Systemic Anaphylaxis. Therefore, we investigated what antibodies, receptors, and cells are involved in active Systemic Anaphylaxis in mice. We found that IgG antibodies, FcγRIIIA and FcγRIV, platelet-activating factor, neutrophils, and, to a lesser extent, basophils were involved. Neutrophil activation could be monitored in vivo during Anaphylaxis. Neutrophil depletion inhibited active, and also passive, Systemic Anaphylaxis. Importantly, mouse and human neutrophils each restored Anaphylaxis in Anaphylaxis-resistant mice, demonstrating that neutrophils are sufficient to induce Anaphylaxis in mice and suggesting that neutrophils can contribute to Anaphylaxis in humans. Our results therefore reveal an unexpected role for IgG, IgG receptors, and neutrophils in Anaphylaxis in mice. These molecules and cells could be potential new targets for the development of Anaphylaxis therapeutics if the same mechanism is responsible for Anaphylaxis in humans.
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IgG-mediated Systemic Anaphylaxis to protein antigen can be induced even under conditions of limited amounts of antibody and antigen
Biochemical and biophysical research communications, 2010Co-Authors: Ryosuke Ishikawa, Yusuke Tsujimura, Kazushige Obata, Yohei Kawano, Yoshiyuki Minegishi, Hajime KarasuyamaAbstract:Systemic Anaphylaxis is an acute, severe, and potentially fatal allergic reaction. Two classes of antibodies, IgE and IgG, contribute to the development of Anaphylaxis in mice, through different mechanisms with distinct usage of effector cells and chemical mediators. Larger quantities of antibody and antigen are reportedly required to induce IgG-mediated Anaphylaxis than IgE-mediated one, suggesting that the former may not happen as frequently as the latter in real life. To readdress this issue, we established in the present study a novel mouse model of passive IgG-mediated Systemic Anaphylaxis to a native protein antigen, ovalbumin (OVA), rather than artificially haptenated protein antigens used in previous studies. Passive sensitization of mice with a cocktail of but not individual IgG1 mAbs specific to distinct OVA epitopes elicited Systemic Anaphylaxis in response to OVA challenge. Importantly, much smaller doses of antibody and antigen than previously reported were sufficient for the induction of IgG-mediated Systemic Anaphylaxis. Moreover, a relatively small dose of antigen could induce severe Anaphylaxis through both IgE- and IgG-mediated mechanisms when mice had been passively sensitized with antigen-specific IgE and IgG. These results strongly suggest that IgG-mediated Systemic Anaphylaxis is not rare among antibody-mediated Systemic Anaphylaxis, in contrast to previous thought, and significantly contributes to active Systemic Anaphylaxis in real life, at least in mice.
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Role for basophils in Systemic Anaphylaxis.
Chemical immunology and allergy, 2010Co-Authors: Hajime Karasuyama, Yusuke Tsujimura, Kazushige Obata, Kaori MukaiAbstract:For more than 100 years since the discovery of basophils by Paul Ehrlich, the functional significance of this rare leukocyte as compared to mast cells has remained an enigma. Studies on basophils have long been hampered by their rarity (less than 1% of peripheral blood leukocytes) and the lack of useful analytical tools such as model animals deficient only in basophils. Recent studies have now defined previously-unrecognized roles for basophils in both allergic responses and immune regulation, and markedly changed our image of basophils, from a neglected minority to a key player in the immune system. We have recently demonstrated that basophils and mast cells play distinct roles in Systemic Anaphylaxis in mice. Basophils are dispensable for IgE-mediated Systemic Anaphylaxis unlike mast cells. Instead, basophils play the major role in IgG-mediated Systemic Anaphylaxis. In vivo depletion of basophils protects mice from anaphylactic death. Upon capture of IgG-allergen complexes, basophils release platelet-activating factor that increases vascular permeability, leading to anaphylactic shock. Thus, there are two major, distinct pathways to allergen-induced Systemic Anaphylaxis: one mediated by basophils, IgG and platelet-activating factor, and the other ‘classical’ pathway mediated by mast cells, IgE and histamine.
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basophils play a pivotal role in immunoglobulin g mediated but not immunoglobulin e mediated Systemic Anaphylaxis
Immunity, 2008Co-Authors: Yusuke Tsujimura, Kazushige Obata, Kaori Mukai, Yohei Kawano, Yoshiyuki Minegishi, Hideo Shindou, Masayuki Yoshida, Hideto Nishikado, Takao Shimizu, Hajime KarasuyamaAbstract:Summary Anaphylaxis is an acute, severe, and potentially fatal Systemic allergic reaction. Immunoglobulin E (IgE), mast cells, and histamine have long been associated with Anaphylaxis, but an alternative pathway mediated by IgG has been suggested to be more important in the elicitation of Anaphylaxis. Here, we showed that basophils, the least common blood cells, were dispensable for IgE-mediated Anaphylaxis but played a critical role in IgG-mediated, passive and active Systemic Anaphylaxis in mice. In vivo depletion of basophils but not macrophages, neutrophils, or NK cells ameliorated IgG-mediated passive Anaphylaxis and rescued mice from death in active Anaphylaxis. Upon capture of IgG-allergen complexes, basophils released platelet-activating factor (PAF), leading to increased vascular permeability. These results highlight a pivotal role for basophils in vivo and contrast two major, distinct pathways leading to allergen-induced Systemic Anaphylaxis: one mediated by basophils, IgG, and PAF and the other "classical" pathway mediated by mast cells, IgE, and histamine.
Toshiaki Shibasaki - One of the best experts on this subject based on the ideXlab platform.
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the effects of fexofenadine on eosinophilia and Systemic Anaphylaxis in mice infected with trichinella spiralis
International Immunopharmacology, 2004Co-Authors: Naohiro Watanabe, Emiko Matsuda, Akiko Masuda, Koichi Nariai, Toshiaki ShibasakiAbstract:Background: The effects of the non-impairing, H1-receptor antagonist fexofenadine were investigated in in vivo mouse models of eosinophilia and Systemic Anaphylaxis. Methods: Eosinophilia was investigated in C57BL/6 mice (n=5 per group) infected with Trichinella spiralis, with and without administration of fexofenadine HCl (5, 10 and 20 mg/kg/day). Eosinophilia was also studied, with and without fexofenadine administration, in mice with a congenital mast-cell deficiency (W/Wv) and controls (+/+). The effect of fexofenadine HCl (20 mg/kg/day) on IL-5 and eotaxin blood levels was also investigated in C57BL/6 mice. In a separate model, Systemic Anaphylaxis was induced in C57BL/6 mice using T. spiralis antigen. Fexofenadine HCl (5, 10 and 20 mg/kg) or vehicle was administered 20 min before antigen challenge (n=5 per group). The effect of fexofenadine on Systemic Anaphylaxis caused by IgE and anti-IgE was also examined in CBF1 mice injected with serum from NC/Nga mice with high IgE levels. Rectal temperature was measured as an indicator of Anaphylaxis. Results: In C57BL/6 mice, repetitive oral administration of fexofenadine HCl (5, 10 and 20 mg/kg/day) resulted in dose-dependent suppression of eosinophilia (p<0.05–0.0001). No suppression was observed in mast-cell deficient W/Wv mice. In addition, single oral administration of fexofenadine HCl (10 and 20 mg/kg) significantly suppressed the decrease in rectal temperature (p<0.01), a marker for Systemic Anaphylaxis, in C57BL/6 mice. In CBF1 mice injected with serum from NC/Nga mice with high IgE levels, the decrease in rectal temperature was suppressed by single administration of fexofenadine HCl (10 and 20 mg/kg; p<0.01 and p<0.001, respectively). Fexofenadine had no effect on peripheral IL-5 and eotaxin levels. Conclusion: These results indicate that fexofenadine suppresses both eosinophilia and Systemic Anaphylaxis, both of which are fundamental reactions in allergic diseases.
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The effects of fexofenadine on eosinophilia and Systemic Anaphylaxis in mice infected with Trichinella spiralis.
International immunopharmacology, 2004Co-Authors: Naohiro Watanabe, Emiko Matsuda, Akiko Masuda, Koichi Nariai, Toshiaki ShibasakiAbstract:Background: The effects of the non-impairing, H1-receptor antagonist fexofenadine were investigated in in vivo mouse models of eosinophilia and Systemic Anaphylaxis. Methods: Eosinophilia was investigated in C57BL/6 mice (n=5 per group) infected with Trichinella spiralis, with and without administration of fexofenadine HCl (5, 10 and 20 mg/kg/day). Eosinophilia was also studied, with and without fexofenadine administration, in mice with a congenital mast-cell deficiency (W/Wv) and controls (+/+). The effect of fexofenadine HCl (20 mg/kg/day) on IL-5 and eotaxin blood levels was also investigated in C57BL/6 mice. In a separate model, Systemic Anaphylaxis was induced in C57BL/6 mice using T. spiralis antigen. Fexofenadine HCl (5, 10 and 20 mg/kg) or vehicle was administered 20 min before antigen challenge (n=5 per group). The effect of fexofenadine on Systemic Anaphylaxis caused by IgE and anti-IgE was also examined in CBF1 mice injected with serum from NC/Nga mice with high IgE levels. Rectal temperature was measured as an indicator of Anaphylaxis. Results: In C57BL/6 mice, repetitive oral administration of fexofenadine HCl (5, 10 and 20 mg/kg/day) resulted in dose-dependent suppression of eosinophilia (p
Toshiyuki Takai - One of the best experts on this subject based on the ideXlab platform.
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The control effect of histamine on body temperature and respiratory function in IgE-dependent Systemic Anaphylaxis
The Journal of allergy and clinical immunology, 2002Co-Authors: Yoko Makabe-kobayashi, Yoshio Hori, Tetsuya Adachi, Satsuki Ishigaki-suzuki, Yoshihiro Kikuchi, Yutaka Kagaya, Kunio Shirato, Andras Nagy, Azusa Ujike, Toshiyuki TakaiAbstract:Abstract Background: The Systemic Anaphylaxis reaction comprises various symptoms, including hypotension, changes in respiration pattern, and hypothermia. Objective: To elucidate the role of histamine in each of these symptoms, we induced the passive Systemic Anaphylaxis reaction in histidine decarboxylase gene knockout (HDC [-/-]) mice, which lack histamine. Methods: HDC(-/-) mice were generated by knocking out the HDC gene, which codes for the unique histamine-synthesizing enzyme. Twenty-four hours after the injection of IgE, HDC(+/+) and HDC(-/-) mice were injected with allergen and body temperature, blood pressure, and respiratory function were monitored in each mouse. Results: Blood pressure dropped in both the HDC(-/-) mice and the HDC(+/+) mice. In contrast, respiratory frequency dropped and the expiratory respiration time was elongated only in the HDC(+/+) mice. Body temperature was decreased in the HDC(+/+) mice and was practically unchanged in the HDC(-/-) mice. Histamine receptor antagonists blocked the body temperature drop in the HDC(+/+) mice. Intravenous histamine induced similar patterns of body temperature decrease in the HDC(+/+) mice and the HDC(-/-) mice. Mast cell-deficient W/W v mice did not show the decrease in body temperature; this suggests that the histamine that contributed to the decrease in body temperature was derived from mast cells. Conclusion: According to the results of this investigation, in the passive Systemic Anaphylaxis reaction, respiratory frequency, expiratory time, and body temperature are shown to be controlled by the activity of histamine, but its contribution to blood pressure is negligible. (J Allergy Clin Immunol 2002;110:298-303.)
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lyn is essential for fcγ receptor iii mediated Systemic Anaphylaxis but not for the arthus reaction
Journal of Experimental Medicine, 2001Co-Authors: Takae Yuasa, Masao Ono, Takeshi Watanabe, Toshiyuki TakaiAbstract:The Src family kinase Lyn initiates intracellular signal transduction by associating with a variety of immune receptors such as antigen receptor on B cells and high-affinity Fc receptor (FcR) for immunoglobulin Ig(E) (FceRI) on mast cells. Involvement of Lyn in the IgE-mediated immediate-type hypersensitivity is well documented, but the physiological significance of Lyn in IgG-dependent, type III low-affinity FcR for IgG (FcγRIII)-mediated responses is largely unknown. In this study, we generated a double-mutant mouse strain deficient in both type II FcR for IgG (FcγRIIB) and Lyn to exclude any involvement of inhibitory signaling by FcγRIIB, which otherwise downregulates FcγRIII-mediated cellular responses. FcγRIIB-deficient but Lyn-sufficient mice served as controls. The Lyn deficiency attenuated IgG-mediated Systemic Anaphylaxis in vivo, and significantly reduced calcium mobilization and degranulation responses of bone marrow–derived mast cells (BMMCs) in vitro. However, we found that either interleukin 4 or tumor necrosis factor α release by BMMCs was comparable to that from Lyn-deficient and control mice, and the reverse-passive Arthus reaction was equally induced in both mutant mice, indicating that Lyn is not involved in the onset of the IgG-mediated, FcγRIII-dependent late phase responses of mast cells. These findings provide us with insight into distinct signaling mechanisms in mast cells underlying the development of diverse pathologies as well as a therapeutic potential for selective treatment of allergic disorders.
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Lyn Is Essential for Fcγ Receptor III–Mediated Systemic Anaphylaxis but Not for the Arthus Reaction
The Journal of experimental medicine, 2001Co-Authors: Takae Yuasa, Masao Ono, Takeshi Watanabe, Toshiyuki TakaiAbstract:The Src family kinase Lyn initiates intracellular signal transduction by associating with a variety of immune receptors such as antigen receptor on B cells and high-affinity Fc receptor (FcR) for immunoglobulin Ig(E) (FceRI) on mast cells. Involvement of Lyn in the IgE-mediated immediate-type hypersensitivity is well documented, but the physiological significance of Lyn in IgG-dependent, type III low-affinity FcR for IgG (FcγRIII)-mediated responses is largely unknown. In this study, we generated a double-mutant mouse strain deficient in both type II FcR for IgG (FcγRIIB) and Lyn to exclude any involvement of inhibitory signaling by FcγRIIB, which otherwise downregulates FcγRIII-mediated cellular responses. FcγRIIB-deficient but Lyn-sufficient mice served as controls. The Lyn deficiency attenuated IgG-mediated Systemic Anaphylaxis in vivo, and significantly reduced calcium mobilization and degranulation responses of bone marrow–derived mast cells (BMMCs) in vitro. However, we found that either interleukin 4 or tumor necrosis factor α release by BMMCs was comparable to that from Lyn-deficient and control mice, and the reverse-passive Arthus reaction was equally induced in both mutant mice, indicating that Lyn is not involved in the onset of the IgG-mediated, FcγRIII-dependent late phase responses of mast cells. These findings provide us with insight into distinct signaling mechanisms in mast cells underlying the development of diverse pathologies as well as a therapeutic potential for selective treatment of allergic disorders.
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Modulation of Immunoglobulin (Ig)E-mediated Systemic Anaphylaxis by Low-Affinity Fc Receptors for IgG
The Journal of experimental medicine, 1999Co-Authors: Azusa Ujike, Yoko Ishikawa, Masao Ono, Takae Yuasa, Tadashi Yoshino, Manabu Fukumoto, Jeffrey V. Ravetch, Toshiyuki TakaiAbstract:It is widely accepted that immunoglobulin (Ig)E triggers immediate hypersensitivity responses by activating a cognate high-affinity receptor, FceRI, leading to mast cell degranulation with release of vasoactive and proinflammatory mediators. This apparent specificity, however, is complicated by the ability of IgE to bind with low affinity to Fc receptors for IgG, FcγRII and III. We have addressed the in vivo significance of this interaction by studying IgE-mediated passive Systemic Anaphylaxis in FcγR-deficient mice. Mice deficient in the inhibitory receptor for IgG, FcγRIIB, display enhanced IgE-mediated anaphylactic responses, whereas mice deficient in an IgG activation receptor, FcγRIII, display a corresponding attenuation of IgE-mediated responses. Thus, in addition to modulating IgG-triggered hypersensitivity responses, FcγRII and III on mast cells are potent regulators of IgE-mediated responses and reveal the existence of a regulatory pathway for IgE triggering of effector cells through IgG Fc receptors that could contribute to the etiology of the atopic response.
Tomoaki Matsumoto - One of the best experts on this subject based on the ideXlab platform.
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Systemic Anaphylaxis after eating storage-mite-contaminated food.
International Archives of Allergy and Immunology, 1996Co-Authors: Tomoaki Matsumoto, Takeshi Hisano, Masamichi Hamaguchi, Teruhisa MiikeAbstract:We describe 2 cases in whom Systemic Anaphylaxis developed shortly after they had eaten food contaminated by a storage mite, Tyrophagus putrescentiae. We were able to demonstrate that these cases were sensitive to the storage mites but not to food allergens, leading us to conclude that the cases' anaphylactic episodes were the result of ingestion of the storage mites. This is the first report of the ingestion of storage mites causing Systemic Anaphylaxis in sensitive persons.
