Department of Food Science and Technology, College of Agriculture and Environmental Sciences, University of California Davis, Davis, CA, USA.
Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, USA.
Environ Toxicol Pharmacol. 2022 Jul;93:103875. doi: 10.1016/j.etap.2022.103875. Epub 2022 May 10.
Chronic exposure to traffic-related air pollution (TRAP) is known to promote systemic inflammation, which is thought to underlie respiratory, cardiovascular, metabolic and neurological disorders. It is not known whether chronic TRAP exposure dampens inflammation resolution, the homeostatic process for stopping inflammation and repairing damaged cells. In vivo, inflammation resolution is facilitated by bioactive lipid mediators known as oxylipins, which are derived from the oxidation of polyunsaturated fatty acids. To understand the effects of chronic TRAP exposure on lipid-mediated inflammation resolution pathways, we measured total (i.e. free+bound) pro-inflammatory and pro-resolving lipid mediators in serum of female rats exposed to TRAP or filtered air (FA) for 14 months. Compared to rats exposed to FA, TRAP-exposed rats showed a significant 36-48% reduction in fatty acid alcohols, specifically, 9-hydroxyoctadecadienoic acid (9-HODE), 11,12-dihydroxyeicosatetraenoic acid (11,12-DiHETE) and 16,17-dihydroxydocosapentaenoic acid (16, 17-DiHDPA). The decrease in fatty acid diols (11,12-DiHETE and 16, 17-DiHDPA) corresponded to a significant 34-39% reduction in the diol to epoxide ratio, a marker of soluble epoxide hydrolase activity; this enzyme is typically upregulated during inflammation. The findings demonstrate that 14 months exposure to TRAP reduced pro-inflammatory 9-HODE concentration and dampened soluble epoxide hydrolase activation, suggesting adaptive immune changes in lipid mediator pathways involved in inflammation resolution.
慢性接触与交通相关的空气污染（TRAP）已知会促进全身炎症，这被认为是呼吸、心血管、代谢和神经紊乱的基础。目前尚不清楚慢性 TRAP 暴露是否会抑制炎症的消退，即停止炎症和修复受损细胞的体内稳态过程。在体内，炎症的消退是由被称为氧化脂类的生物活性脂质介质来促进的，这些介质是由多不饱和脂肪酸的氧化衍生而来的。为了了解慢性 TRAP 暴露对脂质介导的炎症消退途径的影响，我们测量了暴露于 TRAP 或过滤空气（FA）的雌性大鼠血清中的总（即游离+结合）促炎和促解决的脂质介质 14 个月。与暴露于 FA 的大鼠相比，TRAP 暴露的大鼠表现出脂肪酸醇的显著 36-48%降低，具体而言，9-羟基十八碳二烯酸（9-HODE）、11,12-二羟基二十碳四烯酸（11,12-DiHETE）和 16,17-二羟基二十二碳五烯酸（16,17-DiHDPA）。脂肪酸二醇（11,12-DiHETE 和 16,17-DiHDPA）的减少与二醇到环氧化物的比例显著降低 34-39%相对应，这是一种可溶性环氧化物水解酶活性的标志物；这种酶通常在炎症期间上调。这些发现表明，14 个月的 TRAP 暴露降低了促炎的 9-HODE 浓度并抑制了可溶性环氧化物水解酶的激活，这表明参与炎症消退的脂质介质途径中的适应性免疫变化。
