Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.
Front Cell Infect Microbiol. 2022 Mar 23;12:865283. doi: 10.3389/fcimb.2022.865283. eCollection 2022.
Nephropathogenic infectious bronchitis virus (NIBV) is one of the most important viral pathogens in the world poultry industry. Here, we used RT-qPCR, WB and immunofluorescence to explore the interaction between NIBV and the host innate immune system of the kidney. Multiple virions were found in the kidney tissues of the disease group under electron microscopy, and pathological changes such as structural damage of renal tubules and bleeding were observed by HE staining. In addition, we found that the mRNA levels of TLR7, TRAF6, and IKKβ were upregulated after NIBV infection. IRF7 mRNA levels decreased significantly at 5 dpi and increased significantly at 11 to 18 dpi. The NF-κB P65 mRNA level increased significantly at 5 to 18 dpi and decreased at 28 dpi. However, NIBV infection-induced NF-κB P65 protein levels were downregulated at multiple time points. Moreover, we demonstrated that the cytokine (IFN-γ, IL-8, and IL-6) mRNA and protein expression levels were increased significantly at multiple time points after NIBV infection. Furthermore, immunofluorescence analysis showed that NF-κB P65 and IFN-γ were mainly located in the nuclear or perinuclear region. The positive signal intensity of NF-κB P65 was significantly lower than that of the normal group at 1 to 5 dpi, and there was no significant change in the subsequent time period. The positive signal intensity of IFN-γ decreased significantly at 5 dpi, and increased significantly at 11 to 28 dpi. In conclusion, we found that NIBV promoted cytokine release through the TLR7/NF-κB signaling axis, thus causing kidney injury.
肾致病性传染性支气管炎病毒（NIBV）是世界家禽业最重要的病毒病原体之一。在这里，我们使用 RT-qPCR、WB 和免疫荧光技术来探索 NIBV 与宿主肾脏固有免疫系统之间的相互作用。电镜下发现病变组肾脏组织中有多个病毒粒子，HE 染色观察到肾小管结构损伤和出血等病变。此外，我们发现 NIBV 感染后 TLR7、TRAF6 和 IKKβ 的 mRNA 水平上调。IRF7 mRNA 水平在 5 dpi 时显著下降，在 11 至 18 dpi 时显著增加。NF-κB P65 mRNA 水平在 5 至 18 dpi 时显著增加，在 28 dpi 时下降。然而，NIBV 感染诱导的 NF-κB P65 蛋白水平在多个时间点下调。此外，我们证明了细胞因子（IFN-γ、IL-8 和 IL-6）mRNA 和蛋白表达水平在 NIBV 感染后多个时间点显著增加。此外，免疫荧光分析显示 NF-κB P65 和 IFN-γ 主要位于核或核周区域。NF-κB P65 的阳性信号强度在 1 至 5 dpi 时明显低于正常组，随后时间无明显变化。IFN-γ 的阳性信号强度在 5 dpi 时显著降低，在 11 至 28 dpi 时显著增加。总之，我们发现 NIBV 通过 TLR7/NF-κB 信号通路促进细胞因子释放，从而导致肾脏损伤。
