The aggravate effects of fetal exposure to concentrated urban air particles on Th2-associated immune response in male offspring.

浓缩的空气颗粒物（CAPs）已被证明对成年小鼠的免疫系统有加重作用。然而，胎儿暴露于CAP对后代免疫应答的影响尚未阐明。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，然后我们顺序地评估胎儿暴露于CAP对暴露于OVA的雄性后代的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CAP（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）。我们评估了出生后5、10、15和30周的组织学表现、支气管肺泡灌洗液（BALF）中的炎性细胞数量。组织学检查显示，胎仔CAPs暴露引起气道粘膜下层嗜酸性粒细胞和淋巴细胞轻度浸润，并伴有支气管上皮。胎仔暴露于CAP导致巨噬细胞、嗜酸性粒细胞和淋巴细胞显著增加。胎儿暴露于CAP增强了雄性后代的免疫应答。

Concentrated airbone particulate matters (CAPs) has been shown to have an aggravate effect on immune systems in adult mice. However, the effects of fetal exposure to CAPs on immune response in offspring have not been elucidated. 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 CAPs on worsening of allergic manifestations in OVA-exposed male offspring. We administered CAPs (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). We evaluated histological findings, inflammatory cell number in bronchoalveolar lavage fluid (BALF) at ages of 5, 10, 15, and 30 weeks after birth. Histological examination showed that the fetal CAPs exposure caused a slight infiltration of eosinophils and lymphocytes in the submucosa of the airway accompanied in the bronchial epithelium. Fetal exposure to CAPs caused significant increases in macrophage, eosinophil, and lymphocyte. Fetal exposure to CAPs enhanced immune response in male offspring.