Contribution of IL-17 to mouse hepatitis virus strain 3-induced acute liver failure.
10.1007/s11596-012-0095-6
- Author:
Lin ZHU
1
;
Tao CHEN
;
Yulei LU
;
Di WU
;
Xiaoping LUO
;
Qin NING
Author Information
1. Department and Institute of Infectious Diseases, Huazhong University of Science and Technology, Wuhan 430030, China. zl83620@hotmail.com
- Publication Type:Journal Article
- MeSH:
Animals;
Female;
Hepatitis, Viral, Animal;
metabolism;
Interleukin-17;
metabolism;
Liver Failure, Acute;
metabolism;
virology;
Mice;
Mice, Inbred BALB C;
Murine hepatitis virus;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2012;32(4):552-556
- CountryChina
- Language:English
-
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.
