To explore the role of ChTLR4/MyD88/NF-κB signaling pathway on autophagy induced by selenium (Se) deficiency in the chicken bursa of Fabricius, autophagosome formation in the bursa of Fabricius was observed by transmission electron microscopy. Quantitative real-time PCR (qRT-PCR) and Western blot were used to detect the expression of ChTLR4 and its signaling pathway molecules (MyD88, TRIF, and NF-κB), inflammatory factors (IL-1β, IL-8, and TNF-α), and autophagy-related factors (ATG5, Beclin1, and LC3-II) in the Se-deficient chicken bursa of Fabricius at different ages. The results showed that ChTLR4/MyD88/NF-κB signaling pathway was activated in the chicken bursa of Fabricius and autophagy was induced at the same time by Se deficiency. In order to verify the relationship between the autophagy and ChTLR4/MyD88/NF-κB signaling pathway, HD11 cells were used to establish the normal C group, low Se group, and low Se + TLR4 inhibitor (TAK242) group. The results demonstrated that autophagy could be hindered when the TLR4 signaling pathway was inhibited under Se deficiency. Furthermore, autophagy double-labeled adenovirus was utilized to verify the integrity of autophagy flow induced by Se deficiency in HD11 cells. The results showed that it appeared to form a complete autophagy flow under the condition of Se deficiency and could be blocked by TAK242. In summary, we found that Se deficiency was involved in the chicken bursa of Fabricius autophagy occurring by activating the ChTLR4/MyD88/NF-κB pathway.

中文翻译：

---

硒缺乏通过 ChTLR4/MyD88/NF-κB 通路诱导鸡法氏囊自噬。

为探讨ChTLR4/MyD88/NF-κB信号通路在鸡法氏囊缺硒诱导自噬中的作用，采用透射电镜观察法氏囊自噬体的形成。采用定量实时荧光定量 PCR (qRT-PCR) 和蛋白质印迹法检测 ChTLR4 及其信号通路分子（MyD88、TRIF 和 NF-κB）、炎症因子（IL-1β、IL-8 和 TNF）的表达-α) 和自噬相关因子 (ATG5、Beclin1 和 LC3-II) 在不同年龄的法氏缺硒鸡法氏囊中。结果表明，鸡法氏囊中ChTLR4/MyD88/NF-κB信号通路被激活，同时硒缺乏诱导自噬。为了验证自噬与 ChTLR4/MyD88/NF-κB 信号通路的关系，HD11细胞用于建立正常C组、低硒组和低硒+TLR4抑制剂（TAK242）组。结果表明，在硒缺乏的情况下，当 TLR4 信号通路受到抑制时，自噬可能会受到阻碍。此外，利用自噬双标记腺病毒验证了 HD11 细胞中硒缺乏诱导的自噬流的完整性。结果表明，在缺硒条件下，它似乎形成了完整的自噬流，可以被TAK242阻断。总之，我们发现硒缺乏通过激活 ChTLR4/MyD88/NF-κB 通路参与了鸡法氏囊自噬的发生。结果表明，在硒缺乏的情况下，当 TLR4 信号通路受到抑制时，自噬可能会受到阻碍。此外，利用自噬双标记腺病毒验证了 HD11 细胞中硒缺乏诱导的自噬流的完整性。结果表明，在缺硒条件下，它似乎形成了完整的自噬流，可以被TAK242阻断。总之，我们发现硒缺乏通过激活 ChTLR4/MyD88/NF-κB 通路参与了鸡法氏囊自噬的发生。结果表明，在硒缺乏的情况下，当 TLR4 信号通路受到抑制时，自噬可能会受到阻碍。此外，利用自噬双标记腺病毒验证了 HD11 细胞中硒缺乏诱导的自噬流的完整性。结果表明，在缺硒条件下，它似乎形成了完整的自噬流，可以被TAK242阻断。总之，我们发现硒缺乏通过激活 ChTLR4/MyD88/NF-κB 通路参与了鸡法氏囊自噬的发生。结果表明，在缺硒条件下，它似乎形成了完整的自噬流，可以被TAK242阻断。总之，我们发现硒缺乏通过激活 ChTLR4/MyD88/NF-κB 通路参与了鸡法氏囊自噬的发生。结果表明，在缺硒条件下，它似乎形成了完整的自噬流，可以被TAK242阻断。总之，我们发现硒缺乏通过激活 ChTLR4/MyD88/NF-κB 通路参与了鸡法氏囊自噬的发生。