Abstract：
BACKGROUND: Animal models for food allergies serve as crucial tools in understanding allergy mechanisms and assessing the efficacy of potential desensitization methods. The effectiveness of inducing allergies in mice through intragastric lavage sensitization varies. The intraperitoneal method can trigger systemic anaphylaxis, however it lacks anatomical relevance. Hence, a uniform and reliable allergy induction method in mice is required. Tape -stripping can mimic atopic dermatitis (AD), a precursor to lifelong peanut allergies in humans. Furthermore, skin damage triggers the upregulation of skin alarmins and the expansion of small-intestinal mast cells, both implicated in allergy development.
METHODS: We standardized a skin-based sensitization method in a mouse model of peanut allergy using skin tape-stripping followed by allergen application. We compared this method with intragastric sensitization.
RESULTS: Skin-based sensitization led to increased mast cells, goblet cells, and eosinophils in the small intestine, elevated systemic IgE levels, murine mast cell protease-1 (mMCP-1), histamine, and eosinophilic activity in peripheral blood. Moreover, it resulted in a significant hypothermic response, with nearly 30% mortality following an oral challenge one-month post-sensitization.
CONCLUSIONS: Our research offers a standardized and readily reproducible method for inducing peanut allergy in mice, which could also be adapted for other food allergens.
METHODS: We standardized a skin-based sensitization method in a mouse model of peanut allergy using skin tape-stripping followed by allergen application. We compared this method with intragastric sensitization.
RESULTS: Skin-based sensitization led to increased mast cells, goblet cells, and eosinophils in the small intestine, elevated systemic IgE levels, murine mast cell protease-1 (mMCP-1), histamine, and eosinophilic activity in peripheral blood. Moreover, it resulted in a significant hypothermic response, with nearly 30% mortality following an oral challenge one-month post-sensitization.
CONCLUSIONS: Our research offers a standardized and readily reproducible method for inducing peanut allergy in mice, which could also be adapted for other food allergens.
摘要：
背景：食物过敏动物模型是理解过敏机制和评估潜在脱敏方法功效的重要工具。通过灌胃致敏在小鼠中诱导过敏的有效性各不相同。腹膜内方法可以引发全身过敏反应，然而，它缺乏解剖学相关性。因此，在小鼠中需要统一和可靠的过敏诱导方法。胶带剥离可以模拟特应性皮炎（AD），人类终生花生过敏的前兆。此外，皮肤损伤会引发皮肤警报的上调和小肠肥大细胞的扩张，两者都与过敏发展有关。
方法：我们在花生过敏的小鼠模型中标准化了基于皮肤的致敏方法，使用皮肤胶带剥离，然后应用过敏原。我们将这种方法与胃内致敏进行了比较。
结果：皮肤致敏导致肥大细胞增多，杯状细胞,和小肠中的嗜酸性粒细胞，全身IgE水平升高，鼠肥大细胞蛋白酶-1（mMCP-1），组胺,和外周血中的嗜酸性粒细胞活性。此外，它导致了明显的低温反应，致敏后1个月进行口头攻击后死亡率接近30%。
结论：我们的研究为诱导小鼠花生过敏提供了一种标准化且易于重复的方法，也可以适用于其他食物过敏原。
方法：我们在花生过敏的小鼠模型中标准化了基于皮肤的致敏方法，使用皮肤胶带剥离，然后应用过敏原。我们将这种方法与胃内致敏进行了比较。
结果：皮肤致敏导致肥大细胞增多，杯状细胞,和小肠中的嗜酸性粒细胞，全身IgE水平升高，鼠肥大细胞蛋白酶-1（mMCP-1），组胺,和外周血中的嗜酸性粒细胞活性。此外，它导致了明显的低温反应，致敏后1个月进行口头攻击后死亡率接近30%。
结论：我们的研究为诱导小鼠花生过敏提供了一种标准化且易于重复的方法，也可以适用于其他食物过敏原。
