Hyötyläinen Tuulia, Bodin Johanna, Duberg Daniel, Dirven Hubert, Nygaard Unni C, Orešič Matej
School of Science and Technology, Örebro University, Örebro, Sweden.
Division of Infection Control and Environmental Health, Norwegian Institute of Public Health, Oslo, Norway.
Front Genet. 2021 Sep 27;12:721507. doi: 10.3389/fgene.2021.721507. eCollection 2021.
Exposure to Per- and polyfluoroalkyl substances (PFAS) has been linked to multiple undesirable health outcomes across a full lifespan, both in animal models as well as in human epidemiological studies. Immunosuppressive effects of PFAS have been reported, including increased risk of infections and suppressed vaccination responses in early childhood, as well as association with immunotoxicity and diabetes. On a mechanistic level, PFAS exposure has been linked with metabolic disturbances, particularly in lipid metabolism, but the underlying mechanisms are poorly characterized. Herein we explore lipidomic signatures of prenatal and early-life exposure to perfluoroundecanoic acid (PFUnDA) in non-obese diabetic (NOD) mice; an experimental model of autoimmune diabetes. Female NOD mice were exposed to four levels of PFUnDA in drinking water at mating, during gestation and lactation, and during the first weeks of life of female offspring. At offspring age of 11-12 weeks, insulitis and immunological endpoints were assessed, and serum samples were collected for comprehensive lipidomic analyses. We investigated the associations between exposure, lipidomic profile, insulitis grade, number of macrophages and apoptotic, active-caspase-3-positive cells in pancreatic islets. Dose-dependent changes in lipidomic profiles in mice exposed to PFUnDA were observed, with most profound changes seen at the highest exposure levels. Overall, PFUnDA exposure caused downregulation of phospholipids and triacylglycerols containing polyunsaturated fatty acids. Our results show that PFUnDA exposure in NOD mice alters lipid metabolism and is associated with pancreatic insulitis grade. Moreover, the results are in line with those reported in human studies, thus suggesting NOD mice as a suitable model to study the impacts of environmental chemicals on T1D.
全氟和多氟烷基物质(PFAS)的暴露与动物模型以及人类流行病学研究中整个生命周期内的多种不良健康结果相关。已有报道称PFAS具有免疫抑制作用,包括幼儿期感染风险增加和疫苗接种反应受抑制,以及与免疫毒性和糖尿病有关。在机制层面,PFAS暴露与代谢紊乱有关,尤其是脂质代谢,但潜在机制尚不明确。在此,我们探讨了非肥胖糖尿病(NOD)小鼠产前和生命早期暴露于全氟十一烷酸(PFUnDA)的脂质组学特征;NOD小鼠是自身免疫性糖尿病的实验模型。雌性NOD小鼠在交配、妊娠和哺乳期以及雌性后代生命的最初几周,通过饮用水接触四种水平的PFUnDA。在后代11 - 12周龄时,评估胰岛炎和免疫终点,并收集血清样本进行全面的脂质组学分析。我们研究了暴露、脂质组学特征、胰岛炎分级、巨噬细胞数量以及胰岛中凋亡的、活性半胱天冬酶 - 3阳性细胞之间的关联。观察到暴露于PFUnDA的小鼠脂质组学特征呈剂量依赖性变化,在最高暴露水平下变化最为显著。总体而言,PFUnDA暴露导致含有多不饱和脂肪酸的磷脂和三酰甘油下调。我们的结果表明,NOD小鼠暴露于PFUnDA会改变脂质代谢,并与胰腺胰岛炎分级相关。此外,这些结果与人类研究报告的结果一致,因此表明NOD小鼠是研究环境化学物质对1型糖尿病影响的合适模型。