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 NameAffiliationE-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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