ISGylation Inhibits an LPS-Induced Inflammatory Response via the TLR4/NF-κB Signaling Pathway in Goat Endometrial Epithelial Cells.
ISGylation Inhibits an LPS-Induced Inflammatory Response via the TLR4/NF-κB Signaling Pathway in Goat Endometrial Epithelial Cells.
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ISGylation 通过 TLR4/NF-kappa B 信号通路抑制山羊子宫内膜上皮细胞中 LPS 诱导的炎症反应
DOI：
10.3390/ani11092593
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发表时间：
2021-09-03
期刊：
影响因子：
--
通讯作者：
Lin P
中科院分区：
文献类型：
--
作者：
Xiao J;Li S;Zhang R;Wang Z;Zhang X;Wang A;Jin Y;Lin P
子宫内膜炎是家畜常见而重要的生殖疾病，可导致反复不孕、流产、卵巢功能障碍，影响雌性家畜的繁殖率和生产性能，给养殖户造成严重的经济损失。革兰氏阴性菌感染、LPS的释放和TLR 4/NF-κB信号通路的激活是导致该病的主要因素。然而，子宫内膜免疫与细菌感染之间的相互作用机制尚不完全清楚。泛素样蛋白ISG 15通过ISGylation修饰系统调控TLR 4/NF-κB信号通路，进而调节炎症反应。本研究发现ISG 15蛋白主要定位于山羊子宫内膜上皮细胞（gEECs）的胞浆中，且ISG 15修饰的关键基因和蛋白在LPS诱导的gEECs中表达增加。ISG 15基因的过表达和沉默表明ISG化通过TLR 4/NF-κB信号通路抑制gEECs中LPS诱导的炎症反应。本研究为进一步探讨ISGylation修饰系统在子宫内膜炎症反应中的作用及治疗子宫内膜炎提供了实验基础。子宫内膜炎是家畜常见的重要生殖疾病。革兰氏阴性菌感染、脂多糖（LPS）的释放和TLR 4/NF-κB信号通路的激活是导致该病的主要因素。然而，我们并不完全了解子宫内膜免疫和细菌感染之间的相互作用，在疾病的病因。泛素样蛋白ISG 15通过ISGylation修饰系统调控TLR 4/NF-κB信号通路，从而调节炎症反应。在本研究中，我们发现ISG 15蛋白主要表达于山羊子宫内膜上皮细胞（gEECs）的胞浆中，ISG 15的关键基因和蛋白的表达增加LPS诱导的gEECs。ISG 15基因的过表达和沉默表明ISG化通过TLR 4/NF-κB信号通路抑制gEECs中LPS诱导的炎症反应。本研究为进一步探讨ISGylation修饰系统在子宫内膜炎症反应中的作用及治疗子宫内膜炎提供了实验基础。
Endometritis is a common and important reproductive disease of domestic animals, leading to repeated infertility, abortion, and ovarian dysfunction, which affects the reproductive rate and production performance of female domestic animals, and causes serious financial loss to farmers. Infection with Gram-negative bacteria, the release of LPS and activation of the TLR4/NF-κB signaling pathway are the principal factors responsible for the disease. However, the mechanism of the interaction between endometrial immunity and bacterial infection is not entirely clear. Ubiquitin-like protein ISG15 can regulate the TLR4/NF-κB signaling pathway via the ISGylation modification system, which modulates the inflammatory response. In the present study, we found that ISG15 proteins were mainly located in the cytoplasm of goat endometrial epithelial cells (gEECs) and that the expression of key genes and proteins of ISGylation increased in LPS-induce gEECs. Overexpression and silencing of the ISG15 gene demonstrated that ISGylation inhibited an LPS-induced inflammatory response via the TLR4/NF-κB signaling pathway in gEECs. Here, we provide the experimental basis for further exploration of the role of the ISGylation modification system in the inflammatory response of endometrium and a potential method for the treatment of endometritis. Endometritis is a common and important reproductive disease of domestic animals. The principal factors responsible for the disease are infection with Gram-negative bacteria, the release of Lipopolysaccharides (LPS) and activation of the TLR4/NF-κB signaling pathway. However, we do not fully understand the interaction between endometrial immunity and bacterial infection in the disease etiology. The ubiquitin-like protein ISG15 can regulate the TLR4/NF-κB signaling pathway via the ISGylation modification system, modulating the inflammatory response. In the present study, we found that ISG15 protein was expressed mainly in the cytoplasm of goat endometrial epithelial cells (gEECs) and that the expression of key genes and proteins of ISGylation increased in LPS-induced gEECs. Overexpression and silencing of the ISG15 gene demonstrated that ISGylation inhibited an LPS-induced inflammatory response via the TLR4/NF-κB signaling pathway in gEECs. Here, we provide the experimental basis for further exploration of the role of the ISGylation modification system in the inflammatory response of endometrium and a potential method for the treatment of endometritis.
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作者：
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