Institute of Environmental Toxicology, Ibaraki 303-0043, Japan.
Toxicology. 2011 Nov 18;289(2-3):132-40. doi: 10.1016/j.tox.2011.08.003. Epub 2011 Aug 12.
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).
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).
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.
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.
Our results indicate that atopic dermatitis can be aggravated by prior exposure to immunosuppressive environmental chemicals.
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。
本研究的主要目的是研究一些环境化学物质引起的过敏疾病和免疫抑制的发展机制。我们专注于有机磷农药 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（甲氧氯）对用粉尘螨提取物致敏的 NC/Nga 小鼠 AD 的加重作用。
NC/Nga 小鼠在致敏前或致敏同时经口暴露于对硫磷或甲氧氯，然后用粉尘螨进行攻毒。在最后一次攻毒后一天，我们分析了耳软骨的皮炎严重程度和基因表达、血清中的免疫球蛋白（Ig）E 和 IgG（2a）水平，以及耳淋巴结中的 T 或 B 细胞数量和细胞因子产生。
预先暴露于对硫磷或甲氧氯会显著增加以下参数：耳软骨的皮炎严重程度和基因表达、血清中的 IgE 和 IgG（2a）水平、辅助性 T 细胞和 IgE 阳性 B 细胞表面抗原的表达、Th1 和 Th2 细胞因子的产生，以及耳淋巴结细胞中的 IgE 产生。相比之下，同时暴露于对硫磷或甲氧氯会使所有参数最多产生小但显著的降低。
我们的结果表明，特应性皮炎可以通过预先暴露于免疫抑制性环境化学物质而加重。
