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 exacerbates immunological pathology in experimental viral fulminant hepatitis* |
Received:January 09, 2019 Revised:April 25, 2019 |
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KeyWord:MyD88; MHV-3; HMGB1; ILC3 |
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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Abstract: |
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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