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- Title
Selenium Deficiency Causes Inflammatory Injury in the Bursa of Fabricius of Broiler Chickens by Activating the Toll-like Receptor Signaling Pathway.
- Authors
Bai, Yu; Zhang, Ruili; Liu, Qing; Guo, Rong; Li, Guangxing; Sun, Bin; Zhang, Di; Chen, Yang; Huang, Xiaodan
- Abstract
The aim of our study was to observe the effect of selenium (Se) deficiency on inflammatory injury in the bursa of Fabricius of broiler chickens and to determine the role of the Toll-like receptor (TLR)/myeloid differential protein-88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway during this process. Here, we revealed that severe inflammatory injury occurred in the broiler bursa of Fabricius with Se deficiency via histopathology. Moreover, the ultrastructural pathological results showed that the nuclear, mitochondrial, endoplasmic reticulum and cytomembrane structures were damaged to varying degrees. Additionally, interleukin-2 (IL-2), interleukin-6 (IL-6), and interferon (IFN-γ) mRNA expression was markedly upregulated in the broiler bursa of Fabricius with Se deficiency. Furthermore, TLR, toll-interleukin-1 receptor domain-containing adapter-inducing interferon-β (TRIF), MyD88, and NF-κB mRNA expression was also markedly elevated in the broiler bursa of Fabricius with Se deficiency. The above results suggested that Se deficiency increases the expression of numerous proinflammatory cytokines and is probably due to the activation of the TLR/MyD88/NF-κB signaling pathway, which causes inflammatory injury in the bursa of Fabricius of broiler chickens. Our findings provide a theoretical reference for further studying the underlying mechanism of Se deficiency-induced inflammatory injury in the bursa of Fabricius of broiler chickens.
- Subjects
BROILER chickens; TOLL-like receptors; MYELOID differentiation factor 88; SELENOPROTEINS; CELLULAR signal transduction; SELENIUM; ENDOPLASMIC reticulum; INTERFERON receptors
- Publication
Biological Trace Element Research, 2022, Vol 200, Issue 2, p780
- ISSN
0163-4984
- Publication type
Article
- DOI
10.1007/s12011-021-02688-0