Diisononyl phthalate (DINP) is commonly used as a plasticizer in industrial and consumer product applications. Several studies have suggested a possible link between exposure to DINP and the development of allergic asthma, and the synergistic effect of DINP combined with Ovalbumin (OVA) is a possible way to promote an immune response. These findings are still speculative, since there is insufficient evidence to assess the ability of DINP to influence "allergic asthma pathology". This study was designed to determine any effects of OVA/DINP exposure on airway reactivity, particularly when combined with allergen exposure. Experiments to determine these effects were conducted after 15 days of combined exposure and a subsequent challenge with aerosolized ovalbumin for one week. Airway hyper-responsiveness (lung function), lung tissue pathology, cytokines and oxidative stress biomarkers were investigated. We showed that oral exposure to OVA/DINP could induce airway hyper-responsiveness (AHR), and aggravate airway wall remodeling, and that this deterioration was concomitant with increased immunoglobulin-E and Th2 cytokines secretion. The data also demonstrated that DINP could promote oxidative damage in the lung. In summary, this study showed that DINP has an adjuvant effect on allergic asthma affecting lung function, lung histopathology, immune molecules and causes oxidative damage.

中文翻译：

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DINP与OVA的协同或佐剂作用可能是促进免疫反应的机制。

邻苯二甲酸二异壬酯（DINP）通常在工业和消费产品应用中用作增塑剂。多项研究表明，暴露于DINP与过敏性哮喘的发展之间可能存在联系，DINP与卵白蛋白（OVA）的协同作用是促进免疫反应的一种可能方法。这些发现仍然是推测性的，因为没有足够的证据来评估DINP影响“过敏性哮喘病理”的能力。这项研究旨在确定OVA / DINP暴露对气道反应性的任何影响，尤其是与过敏原暴露结合时。联合暴露15天后进行了确定这些效果的实验，随后又用雾化的卵清蛋白攻击了一周。气道高反应性（肺功能），肺组织病理学，细胞因子和氧化应激生物标志物进行了调查。我们发现口服OVA / DINP会引起气道高反应性（AHR），并加剧气道壁重塑，并且这种恶化与免疫球蛋白-E和Th2细胞因子分泌的增加有关。数据还表明，DINP可以促进肺部的氧化损伤。总而言之，这项研究表明，DINP对过敏性哮喘有辅助作用，影响哮喘的肺功能，肺组织病理学，免疫分子并引起氧化损伤。并且这种恶化与免疫球蛋白E和Th2细胞因子分泌的增加同时发生。数据还表明，DINP可以促进肺部的氧化损伤。总而言之，这项研究表明，DINP对过敏性哮喘有辅助作用，影响哮喘的肺功能，肺组织病理学，免疫分子并引起氧化损伤。并且这种恶化与免疫球蛋白E和Th2细胞因子分泌增加有关。数据还表明，DINP可以促进肺部的氧化损伤。总之，这项研究表明，DINP对过敏性哮喘有佐剂作用，影响哮喘的肺功能，肺组织病理学，免疫分子并引起氧化损伤。