A Zinc Chelator TPEN Attenuates Airway Hyperresponsiveness Airway Inflammation in Mice In Vivo
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- Fukuyama Satoru
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Matsunaga Yuko
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Zhanghui Wang
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Noda Naotaka
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Asai Yukari
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Moriwaki Atsushi
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Matsumoto Takafumi
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Nakano Takako
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Matsumoto Koichiro
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Nakanishi Yoichi
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University
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- Inoue Hiromasa
- Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University Present address: Department of Respiratory, Kagoshima University Graduate School of Medical and Dental Sciences
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- タイトル別名
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- A Zinc Chelator TPEN Attenuates Airway Hyperresponsiveness and Airway Inflammation in Mice In Vivo
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Background: Zinc is an essential element required for the cell metabolism, including gene transcription, signal transduction, immunity, and apoptosis. The pathophysiological role of zinc in asthma, however, is not entirely clear. Mast cells have been implicated in atopic asthma, and zinc deprivation has been reported to reduce mast cell activation. Here, we investigate the effects of a zinc chelator, N,N,N',N'-tetrakis (2-pyridyl-methyl) ethylenediamine (TPEN), on asthmatic responses in mouse models of ovalbumin (OVA)-induced airway hyperresponsiveness and allergic airway inflammation.<br> Methods: Mice were sensitized with OVA with or without the adjuvant aluminum hydroxide (alum) and subjected to OVA exposure with or without treatment of TPEN. Cell profiles and cytokine levels in bronchoalveolar lavage (BAL) fluids, airway responsiveness to inhaled acetylcholine, and goblet cell hyperplasia after allergen exposure were assessed.<br> Results: In mice sensitized to OVA without alum, TPEN significantly suppressed airway hyperresponsiveness and eosinophilia in BAL fluids. TPEN also attenuated the upregulation of TNFα, IL-13 and IL-4 in BAL fluids and goblet cell hyperplasia after OVA exposure. By contrast, in mice sensitized to OVA with alum, TPEN suppressed eosinophilia in BAL fluids but not airway hyperresponsiveness and goblet cell hyperplasia.<br> Conclusions: In pulmonary allergic inflammation induced in mice immunized with antigen without alum, zinc chelator inhibits airway inflammation and hyperresponsiveness. These findings suggest that zinc may be a therapeutic target of allergic asthma.<br>
収録刊行物
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- Allergology International
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Allergology International 60 (3), 259-266, 2011
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