Yang Qiao, Shi Yu, Yang Ying, Lou Guohua, Chen Zhi
Department of Infectious Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310016, China.
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Block 6-A, 17th Floor, No. 79 Qingchun Road, Hangzhou, Zhejiang 310003, China ; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, Zhejiang 310003, China.
Mediators Inflamm. 2015;2015:508681. doi: 10.1155/2015/508681. Epub 2015 Mar 29.
Exacerbation of hepatitis B virus-associated liver injury is characterized by abnormal immune response which not only mobilizes specific antiviral effects but also poses a potentially lethal nonspecific sterile inflammation to the host. How nonspecific sterile inflammation is triggered after the preexisting injury caused by specific immune injury remains elusive. In the setting of sterile inflammation, endogenous damage-associated molecular patterns are released by stressed and dying hepatocytes, which alarm the immune system through their potential pattern recognition receptors and related signaling pathways, orchestrate the influx of diverse cytokines, and ultimately amplify liver destruction. This review highlights current knowledge about the sterile hepatic inflammation in the exacerbation of chronic hepatitis B.
乙型肝炎病毒相关肝损伤的加剧以异常免疫反应为特征,这种免疫反应不仅调动特异性抗病毒效应,还会对宿主造成潜在致命的非特异性无菌性炎症。在由特异性免疫损伤导致的先前损伤之后,非特异性无菌性炎症是如何触发的仍不清楚。在无菌性炎症的情况下,应激和濒死的肝细胞会释放内源性损伤相关分子模式,这些分子模式通过其潜在的模式识别受体和相关信号通路警示免疫系统,协调多种细胞因子的流入,并最终加剧肝脏破坏。本综述重点介绍了有关慢性乙型肝炎加剧过程中无菌性肝脏炎症的当前知识。