| Jianzhao Deng,Qin Ning,Weiming Yan,Xuan Yang,Lizhen Zhao,Yuzhang Wu,Bei Zhang. MyD88 exacerbates immunological pathology in experimental viral fulminant hepatitis*. Oncol Transl Med, 2019, 5: 58-67. |
| MyD88可加重实验性病毒性重型肝炎的免疫病理 |
| MyD88 exacerbates immunological pathology in experimental viral fulminant hepatitis* |
| Received:January 09, 2019 Revised:April 25, 2019 |
| DOI： |
| 中文关键词: MyD88基因; MHV-3病毒; HMGB1; ILC3 |
| 英文关键词: MyD88; MHV-3; HMGB1; ILC3 |
| 基金项目:国家自然科学基金项目（面上项目，重点项目，重大项目） |
| Author Name | Affiliation | E-mail | | Jianzhao Deng | Qingdao University | 903807165@qq.com | | Qin Ning | Huazhong University of Science and Technology | | | Weiming Yan | Huazhong University of Science and Technology | | | Xuan Yang | Qingdao University | | | Lizhen Zhao | Qingdao University | | | Yuzhang Wu | Third Military Medical University | | | Bei Zhang* | Qingdao University | zhangbei1245@163.com |
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| 中文摘要: |
| 目的 探讨MyD88信号在MHV-3病毒介导的发病机制中的作用。
方法 本研究对MyD88-/-和WT小鼠的肝脏损伤情况、多种促炎细胞因子和HMGB1的表达情况、炎性ILC3的浸润情况和死亡率进行了评价。
结果 与野生型(WT)小鼠相比，MyD88-/-小鼠感染mhv3后，肝脏中多种促炎细胞因子表达降低，肝脏浸润的ILC3明显减少，导致肝脏病理改变，病毒复制减少，存活时间延长。此外，感染MHV-3后，HMGB1特异性的高表达在被感染的肝细胞/巨噬细胞中，诱导HMGB1蛋白从细胞核迁移到细胞外环境，激活MyD88依赖性炎症。
结论 总的来说，我们的研究结果表明MyD88加重了实验性病毒性重型肝炎的免疫病理。阻断这一信号通路对病毒性重型肝炎的治疗具有重要意义。 |
| 英文摘要: |
| Objective The study aimed to explore the role of MyD88 signaling in MHV-3 virus-mediated fulminant hepatitis.
Methods In this study, we evaluated the lesion status of liver, the expression of multiple pro-inflammatory cytokines and HMGB1, the recruitment of inflammatory ILC3, and the mortality of MyD88-/- and WT mice.
Results The results of our experiments suggest that the expression of multiple pro-inflammatory cytokines causing the recruitment of inflammatory ILC3 to the livers was severely impaired in MyD88-/- mice as compared to wild-type (WT) littermates, resulting in reduced liver pathology, viral replication and prolonged mortality post-infection. Additionally, MHV-3 markedly augments expression of high-mobility group box 1 (HMGB1) in infected hepatocytes/macrophages and induces HMGB1 protein migration from the nucleus to the extracellular milieu, where it activates MyD88-dependent inflammation.
Conclusion Overall, our findings indicate that MyD88 Exacerbates Immunological Pathology in Experimental Viral Fulminant Hepatitis. |
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