Parental PM2.5 Exposure-Promoted Development of Metabolic Syndrome in Offspring Is Associated With the Changes of Immune Microenvironment
Parental PM2.5 Exposure-Promoted Development of Metabolic Syndrome in Offspring Is Associated With the Changes of Immune Microenvironment
复制标题
亲代PM2.5暴露促进子代代谢综合征的发生与免疫微环境的变化有关
DOI：
10.1093/toxsci/kfz109
复制
发表时间：
2019
影响因子：
3.8
通讯作者：
Zhao Jinzhuo
中科院分区：
文献类型：
--
作者：
Zhang Jia;Zeng Xuejiao;Du Xihao;Pan Kun;Song Liying;Song Weimin;Xie Yuquan;Zhao Jinzhuo
父母暴露于环境细颗粒物（PM2.5）与后代的一些不良健康后果有关。尚未评估亲代PM2.5暴露与后代代谢综合征（MetS）发生之间的关联，以及亲代PM2.5暴露对后代小鼠对PM2.5易感性的影响。使用上海-METAS将C57 BL/6亲代小鼠（雄性和雌性小鼠）暴露于过滤空气（FA）或浓缩PM2.5（PM），共16周。在暴露期间的第12周，我们允许亲代雄性和雌性小鼠繁殖后代小鼠。雄性仔鼠随机分为4组，再次暴露于PM和FA。结果表明，无论亲代小鼠是否暴露于PM2. 5，与暴露于FA的子代小鼠相比，暴露于PM2. 5的子代小鼠均出现血压升高、胰岛素抵抗、糖耐量受损和血脂异常。更重要的是，无论后代小鼠暴露于何种环境中，亲代PM暴露都对后代小鼠的空腹血胰岛素、稳态模型评估-胰岛素抵抗、血清低密度脂蛋白胆固醇和总胆固醇、脾脏T辅助细胞17（Th 17）和Treg细胞、血清白细胞介素（IL）-17A，IL-6和IL-10产生了压倒性影响。结果表明，亲代暴露于大气污染可能会诱导子代代谢综合征的发生，并可能增加子代对环境危害的易感性。亲代PM暴露对子代的影响可能与免疫微环境的改变有关。
Parental exposure to ambient fine particulate matter (PM2.5) has been associated with some of adverse health outcomes in offspring. The association between parental PM2.5exposure and the development of metabolic syndrome (MetS) in offspring, and the effects of parental PM2.5exposure on the susceptibility of offspring mice to PM2.5, has not been evaluated. The C57BL/6 parental mice (male and female mice) were exposed to filtered air (FA) or concentrated PM2.5(PM) using Shanghai-METAS for a total of 16 weeks. At week 12 during the exposure, we allowed the parental male and female mice to breed offspring mice. The male offspring mice were divided into 4 groups and exposed to PM and FA again. The results showed that whether the parental mice were exposed to PM2.5or not, the offspring mice exposure to PM2.5appeared the elevation of blood pressure, insulin resistance, impairment of glucose tolerance, and dyslipidemia when compared to the offspring mice exposure to FA. More importantly, no matter what the offspring mice were exposed to, parental PM exposure overwhelmingly impacted the fasting blood insulin, homeostasis model assessment-insulin resistance, serous low-density lipoprotein cholesterol, and total cholesterol, splenic T helper cell 17 (Th17) and Treg cells, serous interleukin (IL)-17A, IL-6, and IL-10 in offspring mice. The results suggested that the parental exposure to air pollution might induce the development of MetS in offspring and might enhance the susceptibility of offspring to environmental hazards. The effects of parental PM exposure on offspring might be related to the changes of immune microenvironment.