皮质醇通过 NF-κB 和 MAPK 信号通路抑制脂多糖诱导的牛子宫内膜基质细胞炎症反应。

Cortisol inhibits lipopolysaccharide-induced inflammatory response in bovine endometrial stromal cells via NF-κB and MAPK signaling pathways.

机构信息

College of Veterinary Medicine, Yangzhou University, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yangzhou, 225009, China; Joint International Research Laboratory of Agriculture and Agri-product Safety of the Ministry of Education, Yangzhou, Jiangsu, 225009, China.

出版信息

Dev Comp Immunol. 2022 Aug;133:104426. doi: 10.1016/j.dci.2022.104426. Epub 2022 Apr 20.

DOI:10.1016/j.dci.2022.104426

PMID:35452691

Abstract

Bovine uterine infection is commonly caused by Escherichia coli (E. coli). Elevated concentrations of plasma cortisol have been reported in postpartum cows. However, the direct role of cortisol in the inflammatory response of bovine endometrial stromal cells (BESCs) remains unclear. Therefore, the aim of the study was to explore the regulatory effect of cortisol on lipopolysaccharide (LPS)-induced inflammatory response in BESCs. Both the primary and immortalized BESCs were used in this study. BESCs were treated with cortisol (5, 15, and 30 ng/mL) in the presence of LPS. The mRNA expression of inflammatory cytokines and chemokines was detected using RT-qPCR. Western blot and immunofluorescence were used to analyze the activation of the NF-κB and MAPK signaling pathways. The results revealed that cortisol downregulated the LPS-induced overexpression of interleukin(IL)-1β, IL-6, IL-8, TNF-α, COX-2, iNOS in BESCs. Moreover, cortisol inhibited LPS-induced phosphorylation levels of IκB, p65, ERK1/2, JNK and p38, and p65 nuclear translocation in BESCs. These results indicated that cortisol inhibited LPS-induced inflammatory response in BESCs, which may be mediated by suppressing the NF-κB and MAPK signaling pathways.

摘要

牛的子宫感染通常由大肠杆菌（Escherichia coli）引起。产后奶牛的血浆皮质醇浓度升高已有报道。然而，皮质醇在牛子宫内膜基质细胞（BESCs）炎症反应中的直接作用尚不清楚。因此，本研究旨在探讨皮质醇对 LPS 诱导的 BESCs 炎症反应的调节作用。本研究使用了原代和永生化的 BESCs。用皮质醇（5、15 和 30ng/mL）处理 BESCs ，同时加入 LPS。使用 RT-qPCR 检测炎症细胞因子和趋化因子的 mRNA 表达。使用 Western blot 和免疫荧光分析 NF-κB 和 MAPK 信号通路的激活。结果表明，皮质醇下调了 LPS 诱导的 BESCs 中白细胞介素（IL）-1β、IL-6、IL-8、TNF-α、COX-2 和 iNOS 的过度表达。此外，皮质醇抑制了 LPS 诱导的 BESCs 中 IκB、p65、ERK1/2、JNK 和 p38 的磷酸化水平，以及 p65 的核转位。这些结果表明，皮质醇抑制了 LPS 诱导的 BESCs 炎症反应，这可能是通过抑制 NF-κB 和 MAPK 信号通路介导的。