title: Contribution of IL-17 to mouse hepatitis virus strain 3-induced acute liver failure.
abstract: Recently, the Th17 cells and IL-17 have been shown to play a critical role in the immune-mediated liver injury in hepatitis B, while their functions in acute liver failure have not been well elucidated yet. In this study, we primarily investigated the role of IL-17 in the development of mouse hepatitis virus strain 3 (MHV-3)-induced acute liver failure. IL-17 mRNA levels in liver tissue were quantified by using quantitative real-time polymerase chain reaction, and cytokine IL-17 levels in liver tissue and serum were determined by using ELISA in MHV-3-induced murine fulminant hepatitis model. The IL-17 expression levels on CD4(+)T and CD8(+)T cells were determined by using flow cytometry. The correlation between IL-17 level and liver injury was studied. Th17 associated cytokines were also investigated by intracellular staining. Our results showed that the IL-17 expression was significantly elevated in the liver and serum of BALB/cJ mice infected with MHV-3. Moreover, a time course study showed that the percentage of both IL-17-producing CD4(+)T cells and IL-17-producing CD8(+)T cells was increased remarkably in the liver starting from 48 h and peaked at 72 h post-infection. There was a close correlation between hepatic or serum IL-17 concentration and the severity of liver injury defined by ALT level, respectively. Th17 associated cytokines, IL-6, IL-21 and IL-22, were also increased significantly at 72 h post-infection. It was concluded that IL-17 may contribute to the pathogenesis of MHV-3-induced acute liver failure.
authors.affiliation: Department and Institute of Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department and Institute of Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.affiliation: Department and Institute of Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Yulei
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Department and Institute of Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Di
authors.initials: D
authors.lastname: Wu
authors.affiliation: Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Luo
authors.affiliation: Department and Institute of Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, China. qning@tjh.tjmu.edu.cn.
authors.forename: Qin
authors.initials: Q
authors.lastname: Ning
mesh_terms: D000818:Animals; D005260:Female; D006524:Hepatitis, Viral, Animal / Q000378:metabolism*; D020381:Interleukin-17 / Q000378:metabolism*; D017114:Liver Failure, Acute / Q000378:metabolism* / Q000821:virology; D051379:Mice; D008807:Mice, Inbred BALB C; D006517:Murine hepatitis virus / Q000378:metabolism*
chemical_list: D020381:Interleukin-17