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A novel mast cell-dependent allergic peritonitis model

机译:一种新型肥大细胞依赖性过敏性腹膜炎模型

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Typical murine models of allergic inflammation are induced by the combination of ovalbumin and aluminum hydroxide. However, accumulating evidence indicates that, in models of asthma and atopic dermatitis, allergic inflammation can be generated in the absence of aluminum hydroxide. Moreover, co-administration of Staphylococcus aureus enterotoxin B with ovalbumin can enhance inflammation. The objective of this study was to establish a rapid and mast cell-dependent murine model of allergic inflammation by inducing allergic peritonitis using ovalbumin and S. aureus enterotoxin B. Allergic peritonitis was induced in C57BL/6 mice by subcutaneous sensitization and intraperitoneal challenge with ovalbumin and S. aureus enterotoxin B. Disease characteristics were assessed by flow cytometry, enzyme-linked immunosorbent assay (ELISA), trypan blue exclusion and colorimetric assays. The time-course of the allergic peritonitis revealed a peak of peritoneal inflammation 48 h after challenge, as assessed by total cells and eosinophil counts. The decrease of cell numbers started 96 h post-challenge, with complete clearance within 168 h. Moreover, significantly higher levels of tryptase and increased vascular permeability were found 30 min following challenge. Allergic inflammation induction by ovalbumin and S. aureus enterotoxin B was impaired in mast cell-deficient mice and partially restored by mice reconstitution with bone marrow-derived mast cells, indicating the mast cell role in this model. We present a novel model of allergic peritonitis that is mast cell-dependent, simple and robust. Moreover, the use of S. aureus enterotoxin B better resembles human allergic inflammation, which is known to be characterized by the colonization of S. aureus.
机译:过敏性炎症的典型小鼠模型是由卵清蛋白和氢氧化铝的组合诱导的。然而,越来越多的证据表明,在哮喘和特应性皮炎的模型中,在没有氢氧化铝的情况下可以产生过敏性炎症。此外,金黄色葡萄球菌肠毒素B与卵清蛋白共同给药可增强炎症。本研究的目的是通过使用卵清蛋白和金黄色葡萄球菌肠毒素 B 诱导过敏性腹膜炎,建立过敏性炎症的快速肥大细胞依赖性小鼠模型。 通过卵清蛋白和金黄色葡萄球菌肠毒素 B 的皮下致敏和腹膜内激发,在 C57BL/6 小鼠中诱导过敏性腹膜炎。 通过流式细胞术评估疾病特征, 酶联免疫吸附测定 (ELISA)、台盼蓝排除和比色测定。过敏性腹膜炎的时间过程显示,在攻击后 48 小时腹膜炎症达到峰值,通过总细胞和嗜酸性粒细胞计数进行评估。细胞数量在攻击后 96 h 开始减少,在 168 小时内完全清除。此外,在攻击后 30 分钟发现类胰蛋白酶水平显着升高,血管通透性增加。卵清蛋白和 S 诱导过敏性炎症。金黄色葡萄球菌肠毒素B在肥大细胞缺陷小鼠中受损,并通过小鼠用骨髓来源的肥大细胞重建而部分恢复,表明肥大细胞在该模型中的作用。我们提出了一种新的过敏性腹膜炎模型,该模型依赖于肥大细胞,简单而稳健。此外,使用金黄色葡萄球菌肠毒素B更类似于人类过敏性炎症,其特征是金黄色葡萄球菌的定植。

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