Establishment of inflammatory model induced by Pseudorabies virus infection in mice
| Autor: | Mei Ling Yu, Ying Yi Wei, Chun Zhi Ren, Ting Jun Hu, Wen Yue Hu, Jin Wu Zhang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
mice
040301 veterinary sciences Swine viruses animal diseases Sus scrofa Pseudorabies Spleen Inflammation inflammatory Proinflammatory cytokine Pseudorabies virus 0403 veterinary science Pathogenesis 03 medical and health sciences Immune system Virology Medicine Animals 030304 developmental biology Swine Diseases 0303 health sciences General Veterinary biology business.industry Interleukin virus diseases 04 agricultural and veterinary sciences biochemical phenomena metabolism and nutrition biology.organism_classification Herpesvirus 1 Suid cytokines Disease Models Animal medicine.anatomical_structure Immunology Tumor necrosis factor alpha Original Article medicine.symptom business |
| Zdroj: | Journal of Veterinary Science |
| ISSN: | 1976-555X 1229-845X |
| Popis: | Background Pseudorabies 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. Objectives 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. Methods 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. Results At 10⁵-10⁶ TCID50 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 TCID50 of PRV produced a significant inflammatory mediator increase. Conclusions An inflammatory model induced by PRV infection was established in mice, and 10² TCID50 PRV was considered as the best concentration for the establishment of the model. |
| Databáze: | OpenAIRE |
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