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首页> 外文期刊>Biochemical and Biophysical Research Communications >Anti-IL-33 antibody treatment inhibits airway inflammation in a murine model of allergic asthma.
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Anti-IL-33 antibody treatment inhibits airway inflammation in a murine model of allergic asthma.

机译:抗IL-33抗体治疗可在变应性哮喘的小鼠模型中抑制气道炎症。

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摘要

Interleukin (IL)-33 is a recently described member of the IL-1 family and has been shown to induce production of T helper type 2 cytokines. In this study, an anti-IL-33 antibody was evaluated against pulmonary inflammation in mice sensitized and challenged with ovalbumin. The anti-IL-33 or a control antibody (150 microg/mouse) was given intraperitoneally as five doses before the sensitization and antigen challenge. Treatment with anti-IL-33 significantly reduced serum IgE secretion, the numbers of eosinophils and lymphocytes, and concentrations of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid compared with administration of a control antibody. Histological examination of lung tissue demonstrated that anti-IL-33 significantly inhibited allergen-induced lung eosinophilic inflammation and mucus hypersecretion. Our data demonstrate for the first time that anti-IL-33 antibody can prevent the development of asthma in a mouse model and indicate that blockade of IL-33 may be a new therapeutic strategy for allergic asthma.
机译:白介素(IL)-33是最近描述的IL-1家族成员,并已显示出可诱导T辅助2型细胞因子的产生。在这项研究中,评估了抗IL-33抗体抵抗卵白蛋白致敏和攻击小鼠的肺部炎症。在致敏和抗原攻击之前,以五剂腹膜内给予抗IL-33或对照抗体(150微克/小鼠)。与给予对照抗体相比,抗IL-33的治疗可显着降低血清IgE分泌,嗜酸性粒细胞和淋巴细胞的数量以及支气管肺泡灌洗液中IL-4,IL-5和IL-13的浓度。肺组织的组织学检查表明,抗IL-33显着抑制了变应原诱导的肺嗜酸性粒细胞炎症和粘液分泌过多。我们的数据首次证明抗IL-33抗体可预防小鼠模型中哮喘的发展,并表明IL-33的阻断可能是过敏性哮喘的一种新的治疗策略。

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