Liu Zhe, Qu Yanpeng, Wang Jianfa, Wu Rui
College of Life Sciences and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing, Heilongjiang, 163319, People's Republic of China.
College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, 2 Xinyang Road, Daqing, Heilongjiang, 163319, People's Republic of China.
Biol Trace Elem Res. 2016 Aug;172(2):465-473. doi: 10.1007/s12011-015-0589-8. Epub 2016 Jan 4.
Selenium (Se) deficiency can cause intestinal mucosal inflammation, which is related to activation of nuclear transcription factor kappa-B (NF-κB) signaling pathway. However, the mechanism of inflammatory response in chicken duodenal mucosa caused by Se deficiency and its relationship with the NF-κB signaling pathway remain elusive. In this study, we firstly obtained Se-deficient chickens bred with 0.01 mg/kg Se and the normal chickens bred with 0.4 mg/kg Se for 35 days. Then, NF-κB signaling pathway, secretory immunoglobulin A (SIgA), inflammatory cytokines, oxidized glutathione, glutathione peroxidase, and glutathione activities were determined. The results showed that Se deficiency obviously enhanced p50, p65, and p65 DNA-binding activities. The phosphorylation of IκB-α and phosphorylation of kappa-B kinase subunit alpha (IKKα) and IKKα were elevated, but IκB-α was decreased (P < 0.05). Moreover, Se deficiency reduced SIgA amount in the duodenal mucosa but increased the level of interleukin-1β (IL-1β), IL-17A, tumor necrosis factor-α (TNF-α), and interferon gamma (IFN-γ). In contrast, anti-inflammatory cytokines, such as TGF-β1 and IL-10, were significantly suppressed. Additionally, Se deficiency increased oxidized glutathione activity, whereas decreased glutathione peroxidase and glutathione activities (P < 0.05), suggesting that Se deficiency affected the regulation function of redox. Taken together, our results demonstrated that Se deficiency attenuated chicken duodenal mucosal immunity via activation of NF-κB signaling pathway regulated by redox activity, which suggested that Se is a crucial host factor involved in regulating inflammation.
硒（Se）缺乏可导致肠道黏膜炎症，这与核转录因子κB（NF-κB）信号通路的激活有关。然而，硒缺乏引起鸡十二指肠黏膜炎症反应的机制及其与NF-κB信号通路的关系仍不清楚。在本研究中，我们首先获得了以0.01 mg/kg硒饲养35天的缺硒鸡和以0.4 mg/kg硒饲养的正常鸡。然后，测定了NF-κB信号通路、分泌型免疫球蛋白A（SIgA）、炎性细胞因子、氧化型谷胱甘肽、谷胱甘肽过氧化物酶和谷胱甘肽活性。结果表明，硒缺乏明显增强了p50、p65和p65的DNA结合活性。IκB-α的磷酸化以及κB激酶亚基α（IKKα）和IKKα的磷酸化升高，但IκB-α降低（P<0.05）。此外，硒缺乏降低了十二指肠黏膜中SIgA的含量，但增加了白细胞介素-1β（IL-1β）、IL-17A、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）的水平。相比之下，抗炎细胞因子，如转化生长因子-β1（TGF-β1）和IL-10，则受到显著抑制。此外，硒缺乏增加了氧化型谷胱甘肽活性，而降低了谷胱甘肽过氧化物酶和谷胱甘肽活性（P<0.05），表明硒缺乏影响了氧化还原的调节功能。综上所述，我们的结果表明，硒缺乏通过氧化还原活性调节的NF-κB信号通路激活减弱了鸡十二指肠黏膜免疫，这表明硒是参与调节炎症的关键宿主因子。
