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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Prior or coinstantaneous oral exposure to environmental immunosuppressive agents aggravates mite allergen-induced atopic dermatitis-like immunoreaction in NC/Nga mice.
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Prior or coinstantaneous oral exposure to environmental immunosuppressive agents aggravates mite allergen-induced atopic dermatitis-like immunoreaction in NC/Nga mice.

机译：先前或同时口服环境免疫抑制剂会加剧NC / Nga小鼠的螨过敏原诱导的特应性皮炎样免疫反应。

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BACKGROUND: Immunosuppressive environmental chemicals may increase the potency of allergens and thereby play a role in the development of allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (AD). OBJECTIVES: This study's primary objective was to examine the mechanisms behind the development of allergic diseases and immunosuppression induced by some environmental chemicals. We focused on the aggravation of AD by the organophosphorus pesticide O,O-diethyl-O-4-nitro-phenylthiophosphate (parathion) and the organochlorine pesticide 1,1,1-trichloro-2,2-bis(4-methoxyphenyl)ethane (methoxychlor), in NC/Nga mice sensitized with extract of Dermatophagoides farinae (Df). METHODS: NC/Nga mice were exposed orally to parathion or methoxychlor prior or coinstantaneous with sensitization with Df. The mice were subsequently challenged with Df. One day after the last challenge with Df, we analyzed dermatitis severity and expression of genes in the ear auricle, immunoglobulin (Ig) E and IgG(2a) levels in serum, and in auricular lymph nodes, T- or B-cell numbers and cytokine production. RESULTS: Prior exposure to parathion or methoxychlor induced marked increases in the following: dermatitis severity and gene expression in the ear auricle, IgE and IgG(2a) levels in serum, expression of surface antigens on helper T-cell and IgE-positive B-cell, production of Th1 and Th2 cytokines, and production of IgE in auricular lymph-node cells. In contrast, coinstantaneous exposure to parathion or methoxychlor yielded, at most, small but significant decreases in all parameters. CONCLUSIONS: Our results indicate that atopic dermatitis can be aggravated by prior exposure to immunosuppressive environmental chemicals.
机译：背景：免疫抑制性环境化学物质可能会增加过敏原的效力，从而在过敏性疾病（如过敏性鼻炎，哮喘和特应性皮炎（AD））的发展中发挥作用。目的：本研究的主要目的是探讨由某些环境化学物质引起的过敏性疾病发展和免疫抑制的背后机制。我们重点研究了有机磷农药O，O-二乙基-O-4-硝基-苯基硫代磷酸酯（对硫磷）和有机氯农药1,1,1-三氯-2,2-双（4-甲氧基苯基）乙烷对AD的加重作用（甲氧基氯），在对法氏皮肤癣菌（Df）提取物致敏的NC / Nga小鼠中。方法：NC / Nga小鼠在暴露于对硫磷或甲氧基氯之前或同时通过Df致敏接触。随后用Df攻击小鼠。在用Df进行最后一次攻击后的一天，我们分析了皮炎的严重程度和耳廓中基因的表达，血清，耳廓淋巴结中的免疫球蛋白（Ig）E和IgG（2a）水平，T细胞或B细胞数量以及细胞因子的产生。结果：事先暴露于对硫磷或甲氧氯中引起的以下症状明显增加：皮炎的严重程度和耳廓中的基因表达，血清中的IgE和IgG（2a）水平，辅助性T细胞和IgE阳性B-上的表面抗原表达细胞，耳垂淋巴结细胞中Th1和Th2细胞因子的产生以及IgE的产生。相反，同时对硫磷或甲氧氯的暴露在所有参数上最多只产生很小但显着的下降。结论：我们的结果表明，事先暴露于免疫抑制性环境化学物质可加剧特应性皮炎。

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