Prior exposure to immunosuppressive organophosphorus or organochlorine compounds aggravates the TH1-and TH2-type allergy caused by topical sensitization to 2,4-dinitrochlorobenzene and trimellitic anhydride
Prior exposure to immunosuppressive organophosphorus or organochlorine compounds aggravates the TH1-and TH2-type allergy caused by topical sensitization to 2,4-dinitrochlorobenzene and trimellitic anhydride
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DOI：
10.3109/1547691x.2011.566231
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发表时间：
2011-06-01
影响因子：
3.3
通讯作者：
Kosaka, Tadashi
中科院分区：
文献类型：
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作者：
Fukuyama, Tomoki;Tajima, Yukari;Kosaka, Tadashi
免疫抑制环境化学物质可能会增加过敏原的效力，从而在过敏性疾病的发展中发挥作用。本研究的主要目的是探讨过敏性疾病与某些环境化学物质诱导的免疫抑制之间关系的机制。本研究以T（H）1型过敏原2，4-二硝基氯苯（DNCB）和T（H）2型过敏原偏苯三酸酐（TMA）为过敏原，研究了有机磷农药O，O-二乙基-O-4-硝基苯硫代磷酸盐（敌百虫）和有机氯农药1，1，1-三氯-2，2-二（4-甲氧基苯基）乙烷（甲氧滴滴涕）对体外和小鼠过敏性的调节作用。对小鼠（4周龄）经口给药氯吡磷或甲氧滴滴涕。末次给药后4周，对小鼠进行DNCB或TMA致敏，并测量其T淋巴细胞增殖（使用局部淋巴结试验[LLNA]）。此外，我们通过0.1%DNCB或0.3%TMA处理后耳淋巴结中的表面抗原表达和局部细胞因子产生来分析T淋巴细胞。DNCB和TMA的估计浓度，以产生一个刺激指数（SI）的细胞增殖的三个显着下降，在敌百虫和甲氧氯预处理的小鼠。农药预处理诱导淋巴结细胞中辅助和细胞毒性T细胞数量、T（H）1和T（H）2细胞因子水平以及基因表达显著增加。根据我们的研究结果，T（H）1型和T（H）2型过敏因先前暴露于免疫抑制环境化学物质而加重。
Immunosuppressive environmental chemicals may increase the potency of allergens and thereby play a role in the development of allergic diseases. This study''s primary objective was to examine the mechanisms behind the relationship between allergic diseases and the immunosuppression induced by some environmental chemicals. We focused on the modulation of allergic potential in vitro and in mice by the organophosphorus pesticide O,O-diethyl-O-4-nitrophenyl-thiophosphate (parathion) and the organochlorine pesticide 1,1,1-trichloro-2,2-bis(4-methoxy-phenyl)ethane (methoxychlor), with respect to the T(H)1-type allergen 2,4-dinitrochlorobenzene (DNCB) and the T(H)2-type allergen trimellitic anhydride (TMA). Mice (4-week-old) were orally administered parathion or methoxychlor. Four weeks after the final dosing, the mice were sensitized to DNCB or TMA, and T-lymphocyte proliferation measured in their (using a local lymph node assay [LLNA]). In addition, we analyzed T-lymphocytes via surface antigen expression and local cytokine production in auricular lymph nodes after treatment with 0.1% DNCB or 0.3% TMA. The estimated concentration of DNCB and TMA to yield a stimulation index (SI) of cell proliferation of three decreased markedly in parathion- and methoxychlor-pre-treated mice. Pesticide pre-treatment induced marked increases in the number of helper and cytotoxic T-cells, levels of T(H)1 and T(H)2 cytokines, and gene expression in lymph node cells. According to our results, T(H)1- and T(H)2-type allergies are aggravated by prior exposure to immunosuppressive environmental chemicals.