College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, People's Republic of China.
Food Funct. 2020 Jul 1;11(7):6467-6475. doi: 10.1039/d0fo00394h. Epub 2020 Jul 3.
Selenium (Se) is an essential trace element and its deficiency can lead to immune dysfunction. Many studies have investigated the immune damage caused by Se deficiency in chickens, but its mechanism still needs to be explored. In this study, we fed 1-day-old Hyline male chickens with Se deficient diets (the Se content was 0.008 mg kg of diet) and a basal diet (the Se content was 0.15 mg kg of diet). The spleen was collected at the sixth week and used for subsequent experiments. The pathological analysis showed that Se deficiency leads to the destruction of the normal nuclear structure of the spleen cell, and we can observe obvious chromatin condensation and nuclear debris. We constructed a transcriptome database and analyzed the abundance of various genes in the spleen by transcriptome sequence. The analysis of differentially expressed genes (DEGS) showed significant changes in 337 genes, including 210 up-regulations and 127 down-regulations after feeding Se deficient diets. Se deficiency can significantly change oxidative stress and inflammatory response genes in chicken spleen. This study confirmed that Se deficiency increased the IL-2 levels, whereas it down-regulated IL-17, IFN-γ and Foxp3, which indicates that the immune dysfunction of the spleen and Th1/Th2 is imbalanced. We also found that Se deficiency down-regulated some related genes for endoplasmic reticulum Ca transport, leading to endoplasmic reticulum stress (ERS). Moreover, we determined that Se deficiency triggered the low expression of DUSP1/NF-κB. In summary, our results indicate that Se deficiency can inhibit the spleen immune function of chickens by regulating the DUSP1/NF-κB pathway and ERS, leading to spleen damage in chickens. Based on transcriptomics research, our results will help further study the harmful effects of Se deficiency.
硒（Se）是一种必需的微量元素，其缺乏可导致免疫功能障碍。许多研究已经调查了硒缺乏对鸡的免疫损伤，但仍需要探索其机制。在这项研究中，我们用含硒量为 0.008mg/kg 日粮的低硒饲料和含硒量为 0.15mg/kg 日粮的基础饲料喂养 1 日龄海兰雄性小鸡。第六周采集脾脏进行后续实验。病理学分析表明，硒缺乏导致脾细胞核正常结构破坏，可观察到明显的染色质浓缩和核碎片。我们构建了转录组数据库，并通过转录组序列分析了脾脏中各种基因的丰度。差异表达基因（DEGS）分析显示，饲喂低硒饲料后，有 337 个基因的丰度发生显著变化，其中 210 个上调，127 个下调。硒缺乏可显著改变鸡脾脏中的氧化应激和炎症反应基因。本研究证实，硒缺乏可增加 IL-2 水平，而降低 IL-17、IFN-γ 和 Foxp3，表明脾脏和 Th1/Th2 的免疫功能障碍失衡。我们还发现，硒缺乏下调了一些与内质网 Ca 转运相关的基因，导致内质网应激（ERS）。此外，我们确定硒缺乏触发了 DUSP1/NF-κB 的低表达。总之，我们的研究结果表明，硒缺乏可通过调节 DUSP1/NF-κB 通路和 ERS 抑制鸡的脾脏免疫功能，导致鸡脾脏损伤。基于转录组学研究，我们的结果将有助于进一步研究硒缺乏的有害影响。
