Navuluri Lalitha, Parvataneni Sitaram, Hassan Hanem, Birmingham Neil P, Kelly Caleb, Gangur Venu
Food Allergy and Immunology Laboratory, Department of Food Science and Human Nutrition, Nutritional Immunology Program, Michigan State University, East Lansing, Mich. 48824, USA.
Int Arch Allergy Immunol. 2006;140(3):270-6. doi: 10.1159/000093284. Epub 2006 May 11.
Allergy to sesame seeds is an emerging food allergy of a serious nature due to a high risk of systemic anaphylaxis. Although a mouse model to study sesame anaphylaxis is desirable, currently it is not available. Here, using a transdermal exposure model system, we tested the hypothesis that sesame seed elicits IL-4-associated IgE antibody response with consequent clinical sensitization in mice.
Groups of BALB/c mice were exposed to sesame seed extract or saline or a control food (vanilla bean extract) by transdermal applications. Systemic IgE, IgG1 and IgG2a antibody responses were examined using preoptimized ELISA. Type 2 and type 1 cytokine responses were evaluated by ex vivo antigen-mediated activation of spleen cells. Clinical response to oral sesame challenge was studied. Western blot and N-terminal amino acid sequence analyses were performed to identify the sesame allergens.
Transdermal exposure to sesame elicited robust IgE and IgG1 but very little IgG2a antibody responses. IgE response to transdermal exposure in two high-IgE responder mice strains with disparate MHC confirmed the intrinsic allergenicity of sesame seed. Transdermal sensitization was associated with activation of IL-4 but not IFN-gamma. Furthermore, oral exposure to sesame resulted in clinical signs of systemic anaphylaxis. Western blot and sequence analysis identified four allergens including Ses i 3 and the basic subunit of 11s globulins.
These data argue that transdermal exposure to sesame seed can result in IL-4 activation, IgE response and clinical sensitization for systemic anaphylaxis.
由于全身性过敏反应风险高,芝麻过敏是一种新出现的严重食物过敏。尽管需要一个研究芝麻过敏反应的小鼠模型,但目前尚无可用模型。在此,我们使用经皮暴露模型系统,检验了芝麻引发与白细胞介素-4相关的IgE抗体反应并导致小鼠临床致敏的假说。
将BALB/c小鼠分组,通过经皮应用给予芝麻提取物、生理盐水或对照食物(香草豆提取物)。使用预先优化的酶联免疫吸附测定法检测全身性IgE、IgG1和IgG2a抗体反应。通过体外抗原介导的脾细胞激活评估2型和1型细胞因子反应。研究口服芝麻激发试验的临床反应。进行蛋白质印迹和N端氨基酸序列分析以鉴定芝麻过敏原。
经皮暴露于芝麻引发强烈的IgE和IgG1抗体反应,但IgG2a抗体反应非常少。在两种具有不同主要组织相容性复合体的高IgE反应小鼠品系中,对经皮暴露的IgE反应证实了芝麻种子的内在致敏性。经皮致敏与白细胞介素-4的激活有关,但与干扰素-γ无关。此外,口服芝麻导致全身性过敏反应的临床症状。蛋白质印迹和序列分析鉴定出四种过敏原,包括Ses i 3和11s球蛋白的碱性亚基。
这些数据表明,经皮暴露于芝麻种子可导致白细胞介素-4激活、IgE反应和全身性过敏反应的临床致敏。