The aggravate effects of fetal exposure to urban particulate matter on immune system in male offspring

产前暴露于大气颗粒物（CAPs）对雄性后代的免疫系统有严重影响。然而，对机制知之甚少。在本研究中，我们通过将后代暴露于卵清蛋白（OVA）来建立支气管哮喘小鼠模型，然后我们依次评估胎儿暴露于两种类型的颗粒（CAP和亚洲沙尘）对暴露于OVA的雄性后代过敏表现恶化的影响。我们在妊娠第7天和第14天通过阴道内注射将颗粒（200μg/动物）给予妊娠期间的母鼠。9和24周龄的雄性后代用OVA进行气管内注射（4次，间隔2周）。CAPs和亚洲沙尘显著增加BALF中细胞因子和趋化因子的水平。我们的研究结果表明，胎儿暴露于CAP和亚洲沙尘和出生后的卵清蛋白的intraperitheal管理增强过敏性肺部炎症通过激活Th 2相关的免疫反应，通过增加细胞因子和趋化因子，这在支气管哮喘中发挥重要作用。我们的研究结果表明，孕妇吸入CAPs和亚洲沙尘对胎儿有各种影响，并可能与儿童过敏的患病率增加有关。

Prenatal exposure of concentrated airbone particulate matters (CAPs) has been shown to have an aggravate effect on immune system in male offspring. However, little is known about the mechanisms. In the present study we created a bronchial asthma mouse model by exposing offspring to ovalbumin (OVA), then we sequentially evaluated the effects of fetal exposure to two type of particles (CAPs and Asian sand dust) on worsening of allergic manifestations in OVA-exposed male offspring. We administered particle (200μg/animal) by intratracheal injection into dams during pregnancy on days 7 and 14 of gestation. Nine and twenty-four week-old male offspring were injected intratracheally with OVA (4 times at 2-week intervals). CAPs and Asian sand dust significantly increased the level of cytokine and chemokine levels in BALF. Our results suggest that fetal exposure to CAPs and Asian sand dust and postnatal intratracheal administration of OVA enhance allergic lung inflammation by activating the Th2-associated immune response through increase in cytokines and chemokines, which play an important role in bronchial asthma. Our findings suggest that the inhalation of CAPs and Asian sand dust by pregnant women has various effects on the fetus and may be involved in the increased prevalence of childhood allergies.