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.
Keywords: Chicken; Duodenal mucosa; NF-κB; Se deficiency.