College of Animal Science and Technology, Guangxi University, Nanning 530004, PR China.
Guangxi Agricultural Vocational College, Nanning 530007, PR China.
J Vet Sci. 2021 Mar;22(2):e20. doi: 10.4142/jvs.2021.22.e20.
virus (PRV) infection leads to high mortality in swine. Despite extensive efforts, effective treatments against PRV infection are limited. Furthermore, the inflammatory response induced by PRV strain GXLB-2013 is unclear.
Our study aimed to investigate the inflammatory response induced by PRV strain GXLB-2013, establish an inflammation model to elucidate the pathogenesis of PRV infection further, and develop effective drugs against PRV infection.
Kunming mice were infected intramuscularly with medium, LPS, and different doses of PRV-GXLB-2013. Viral spread and histopathological damage to brain, spleen, and lung were determined at 7 days post-infection (dpi). Immune organ indices, levels of reactive oxygen species (ROS), nitric oxide (NO), and inflammatory cytokines, as well as levels of activity of COX-2 and iNOS were determined at 4, 7, and 14 dpi.
At 10⁵-10⁶ TCID PRV produced obviously neurological symptoms and 100% mortality in mice. Viral antigens were detectable in kidney, heart, lung, liver, spleen, and brain. In addition, inflammatory injuries were apparent in brain, spleen, and lung of PRV-infected mice. Moreover, PRV induced increases in immune organ indices, ROS and NO levels, activity of COX-2 and iNOS, and the content of key pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α, interferon-γ and MCP-1. Among the tested doses, 10² TCID of PRV produced a significant inflammatory mediator increase.
An inflammatory model induced by PRV infection was established in mice, and 10² TCID PRV was considered as the best concentration for the establishment of the model.
病毒（PRV）感染导致猪的死亡率很高。尽管进行了广泛的努力，但针对 PRV 感染的有效治疗方法仍然有限。此外，PRV 株 GXLB-2013 诱导的炎症反应尚不清楚。
本研究旨在探讨 PRV 株 GXLB-2013 诱导的炎症反应，建立炎症模型以进一步阐明 PRV 感染的发病机制，并开发针对 PRV 感染的有效药物。
昆明小鼠肌肉注射中等剂量、LPS 和不同剂量的 PRV-GXLB-2013。感染后 7 天（dpi）检测病毒在脑、脾和肺中的传播及组织病理学损伤。在 4、7 和 14 dpi 时检测免疫器官指数、活性氧（ROS）、一氧化氮（NO）和炎症细胞因子水平，以及 COX-2 和 iNOS 的活性。
10⁵-10⁶ TCID 的 PRV 可导致小鼠出现明显的神经症状和 100%的死亡率。病毒抗原可在肾、心、肺、肝、脾和脑中检测到。此外，PRV 感染的小鼠脑、脾和肺均出现明显的炎症损伤。此外，PRV 诱导免疫器官指数、ROS 和 NO 水平、COX-2 和 iNOS 活性以及关键促炎细胞因子（白细胞介素（IL）-1β、IL-6、肿瘤坏死因子-α、干扰素-γ和单核细胞趋化蛋白-1）含量增加。在测试的剂量中，10² TCID 的 PRV 引起了明显的炎症介质增加。
成功建立了 PRV 感染诱导的小鼠炎症模型，10² TCID 的 PRV 被认为是建立该模型的最佳浓度。
