Jiang Kangfeng, Chen Xiuying, Zhao Gan, Wu Haichong, Mi Junxian, Qiu Changwei, Peng Xiuli, Deng Ganzhen
1 Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University , Wuhan, People's Republic of China .
2 Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Ministry of Education, Huazhong Agricultural University , Wuhan, People's Republic of China .
J Interferon Cytokine Res. 2017 Feb;37(2):81-89. doi: 10.1089/jir.2016.0058. Epub 2016 Nov 15.
Interferon-tau (IFN-τ) is a type I interferon and considered as a pregnancy recognition signal in ruminants. Our previous reports have confirmed that IFN-τ has a potential anti-inflammatory effect in macrophage. However, the anti-inflammatory effect of IFN-τ on endometritis has never been reported. Thus, the aim of this study was to investigate the effects of IFN-τ in a mouse model of Staphylococcus aureus-induced endometritis. The histopathological and myeloperoxidase activity results showed that IFN-τ could protect the uterus from S. aureus damage. Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction results revealed that IFN-τ inhibited TNF-α, IL-1β, and IL-6 production. TLR2, involved in the S. aureus infection, was downregulated by IFN-τ and directly activated nuclear transcription factor kappa-B (NF-κB) pathway. Then, we measured the phosphorylation of IκBα and NF-κB p65 by Western blotting. Western blotting results indicated that IFN-τ inhibited the phosphorylation of IκBα and NF-κB p65 in the S. aureus-induced endometritis. Matrix metalloproteinase (MMP)9, which has been reported to be regulated by NF-κB, was also suppressed by IFN-τ, but its inhibitors, tissue inhibitor of metalloproteinases1 level, increased. All of these findings suggested that IFN-τ plays an anti-inflammatory role in S. aureus-induced endometritis by suppressing NF-κB pathway and MMP9 expression.
干扰素 -τ（IFN-τ）是一种I型干扰素，被认为是反刍动物的妊娠识别信号。我们之前的报告证实，IFN-τ在巨噬细胞中具有潜在的抗炎作用。然而，IFN-τ对子宫内膜炎的抗炎作用尚未见报道。因此，本研究的目的是在金黄色葡萄球菌诱导的子宫内膜炎小鼠模型中研究IFN-τ的作用。组织病理学和髓过氧化物酶活性结果表明，IFN-τ可以保护子宫免受金黄色葡萄球菌的损伤。酶联免疫吸附测定和定量实时聚合酶链反应结果显示，IFN-τ抑制肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的产生。参与金黄色葡萄球菌感染的Toll样受体2（TLR2）被IFN-τ下调，并直接激活核转录因子κB（NF-κB）通路。然后，我们通过蛋白质免疫印迹法检测IκBα和NF-κB p65的磷酸化。蛋白质免疫印迹结果表明，IFN-τ在金黄色葡萄球菌诱导的子宫内膜炎中抑制IκBα和NF-κB p65的磷酸化。据报道受NF-κB调节的基质金属蛋白酶（MMP）9也被IFN-τ抑制，但其抑制剂金属蛋白酶组织抑制剂1水平升高。所有这些发现表明，IFN-τ通过抑制NF-κB通路和MMP9表达在金黄色葡萄球菌诱导的子宫内膜炎中发挥抗炎作用。
